Professional Documents
Culture Documents
Epidemiology
EDITORIAL.p65
21
5/6/2003, 9:57 AM
EDITORIAL.p65
22
5/6/2003, 9:57 AM
EDITORIAL.p65
23
5/6/2003, 9:57 AM
EDITORIAL.p65
24
5/6/2003, 9:57 AM
EDITORIAL.p65
25
5/6/2003, 9:57 AM
41.
42.
43.
44.
45.
46.
47.
48.
49.
EDITORIAL.p65
26
50.
51.
52.
53.
54.
55.
56.
5/6/2003, 9:57 AM
IHJ-328-02.p65
27
5/6/2003, 9:58 AM
Table 1. Evidence favoring the role of CMV and other herpesviridae in atherogenesis
Reference
Year
Number of
subjects (n)
Findings
Grattan et al.16
1989
301
Zhu et al.17
2000
238
Muhlestein et al.18
2000
985
Siscovick et al.19
2000
213
Horvath et al.20
2000
244
Sorlie et al.21
2000
515
Kaftan et al.22
1999
310
Neumann et al.23
2000
551
Biocina et al.24
1999
284
Blum et al.25
1998
65
Zhou et al.26
1996
75
Alber et al.27
2000
NA
Lemstrom et al.28
1997
NA
Zhou et al.29
1999
60
Lin et al.30
2000
40
CMV: cytomegalovirus; HSV: herpes simplex virus; CRP: C-reactive protein; CAD: coronary artery disease; CHD: coronary heart disease; apo E: apolipoprotein
E; IHD: ischemic heart disease
IHJ-328-02.p65
28
5/6/2003, 9:58 AM
Year
Number of
subjects (n)
Findings
Mendall et al.31
Patel et al.32
1994
1995
200
388
Gunn et al.33
2000
556
Kahan et al.34
Farsak et al.35
2000
2000
200
85
Hoffmeister et al.36
2001
405
Pieniazek et al.37
Ameriso et al.38
Laurila et al.39
1999
2001
1999
157
38
880
Markus et al.40
Birnie et al.41
1998
1998
357
136
100
H. pylori: Helicobacter pylori; CAD: coronary artery disease; AMI: acute myocardial infarction; HDL: high-density lipoprotein
IHJ-328-02.p65
29
5/6/2003, 9:58 AM
Year
Number of
subjects (n)
Findings
Hu et al.42
Muhlestein et al.43
1999
1998
40
30
Liu et al.44
2000
NA
Kuo et al.45
1993
36
Muhlestein et al.46
1996
114
Ericson et al.47
2000
60
Maass et al.48
1998
70
Bartels et al.49
1999
58
Farsak et al.35
2000
85
Ouchi et al.50
2000
177
Saikku et al.51
1998
213
Gabriel et al.52
1998
282
Toss et al.53
1998
256
Melnick et al.54
1993
300
Burian et al.55
2001
405
Leowattana et al.56
2000
243
Maass et al.57
2000
188
Kaftan et al.58
2000
160
Sessa et al.59
1999
228
Wong et al.60
Dechend et al.61
1999
1999
804
NA
Fong62
2000
NA
C. pneumoniae: Chlamydia pneumomiae; CAD: coronary artery disease; AMI: acute myocardial infarction; LDL: low-density lipoprotein; CRP: C-reactive
protein; HDL: high-density lipoprotein; PCR: polymerase chain reaction; PAI: plasminogen activator inhibitor
IHJ-328-02.p65
30
5/6/2003, 9:58 AM
IHJ-328-02.p65
31
5/6/2003, 9:58 AM
IHJ-328-02.p65
32
5/6/2003, 9:58 AM
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
IHJ-328-02.p65
33
5/6/2003, 9:58 AM
IHJ-328-02.p65
34
76.
77.
78.
79.
80.
81.
82.
83.
84.
85.
86.
87.
88.
5/6/2003, 9:58 AM
Background: The goal of this study was to evaluate the utility of plasma N-terminal pro-brain natriuretic
peptide for the diagnosis of heart failure in patients presenting with shortness of breath.
Methods and Results: We measured plasma levels of N-terminal pro-brain natriuretic peptide in 119 patients
presenting with shortness of breath. The patients were divided into two groups based on the Framingham criteria
and echocardiographic resultsthose with heart failure and those not in heart failure. Plasma levels of
N-terminal pro-brain natriuretic peptide were compared in the two groups. The mean N-terminal pro-brain
natriuretic peptide concentration in patients with heart failure (n=73) was higher than that in those not in
heart failure (389148 fmol/ml v. 14254 fmol/ml, p<0.001). N-terminal pro-brain natriuretic peptide values
increased significantly as the functional severity of heart failure increased (p<0.001). The mean N-terminal
pro-brain natriuretic peptide levels were 26134 fmol/ml for patients in New York Heart Association functional
class I, 300161 fmol/ml for patients in New York Heart Association functional class II, 427103 fmol/ml for
patients in New York Heart Association functional class III and 528170 fmol/ml for patients in New York
Heart Association functional class IV. Using a cut-off value of 200 fmol/ml, the sensitivity of N-terminal
pro-brain natriuretic peptide was 97%, specificity was 89% and accuracy for differentiating heart failure from
other causes of shortness of breath was 93%.
Conclusions: Our results suggest that N-terminal pro-brain natriuretic peptide can be reliably used for the
diagnosis of heart failure in an outpatient setting, and this will improve the ability of clinicians to differentiate
patients with shortness of breath due to heart failure from those with other causes of shortness of breath.
(Indian Heart J 2003; 55: 3539)
Key Words: Heart failure, Natriuretic peptide, Echocardiography
IHJ-378-02.p65
35
5/6/2003, 9:59 AM
IHJ-378-02.p65
36
Characteristics
No heart failure
n=46 (38.7%)
53.3511.62
51 (69.8)
54.2613.37
27 (58.6)
33 (45.2)
27 (36.9)
28 (38.3)
31 (42.4)
16 (34.7)
14 (30.7)
6 (13.0)
26 (56.5)
73 (100)
42 (57.5)
16 (21.9)
46 (100)
3 (6.5)
11 (23.9)
49 (67.1)
50 (68.4)
52 (71.2)
36 (49.3)
26 (35.6)
44 (60.2)
17 (36.9)
11 (23.9)
5 (10.8)
2 (4.3)
15 (32.6)
9 (19.5)
MI: myocardial infarction; JVP: jugular venous pressure; CXR: chest X-ray
5/6/2003, 9:59 AM
IHJ-378-02.p65
37
Fig. 3. Scatter plot showing the correlation of the left ventricular ejection
fraction (LVEF) with plasma levels of N-terminal pro-brain natriuretic peptide
(NT-proBNP). There was a significant negative linear correlation between LVEF
and NT-proBNP.
5/6/2003, 9:59 AM
Fig. 4. Receiveroperating characteristics curve for various cut-off levels of Nterminal pro-brain natriuretic peptide for the diagnosis of heart failure. The
number in parenthesis is the 95% confidence interval. AUC: area under the
receiveroperating characteristics curve
Odds ratio
95% CI
p value
1.8
2.86
3.08
6.55
8.8
8.94
11.34
1.202.730
1.674.900
1.665.690
2.8215.18
2.9026.81
3.920.48
2.8644.87
0.001
<0.001
<0.001
<0.001
<0.001
<0.001
<0.001
CI: confidence interval; JVP: jugular venous pressure; NT-proBNP: Nterminal pro-brain natriuretic peptide
Discussion
Our study was designed to assess the diagnostic value of
the plasma level of circulating NT-proBNP as a noninvasive
indicator of HF. Our results suggest that NT-proBNP can
be used as a reliable marker for identification of left
ventricular dysfunction in a group of patients presenting
with shortness of breath. We found that a cut-off value of
200 fmol/ml had an accuracy of 93%.
Echocardiography, although currently the gold standard
for the diagnosis of left ventricular dysfunction, is costly
and has limited availability in an urgent care setting.
Dyspneic patients may be unable to hold their breath long
IHJ-378-02.p65
38
5/6/2003, 9:59 AM
9.
10.
11.
12.
13.
References
1. Cheitlin MD, Zipes DP. Cardiovascular disease in special population.
In: Braunwald E, Zipes DP, Libby P (eds). Heart disease: a text book of
cardiovascular medicine. 6th ed. Philadelphia: WB Saunders Co; 2001.
p. 2019
2. Kannel WB, Belanger AJ. Epidemiology of heart failure. Am Heart J
1991; 121: 951957
3. OConnell JB, Bristow MR. Economic impact of heart failure in the
United States: time for a different approach. J Heart Lung Transplant
1994; 13 (Suppl): S107S112
4. Dao Q, Krishnaswamy P, Kazanegra R, Harrison A, Amirnovin R,
Lenert L, et al. Utility of B-type natriuretic peptide in the diagnosis of
congestive heart failure in an urgent-care setting. J Am Coll Cardiol
2001; 37: 379385
5. Nagagawa O, Ogawa Y, Itoh H, Suga S, Komatsu Y, Kishimoto I, et al.
Rapid transcriptional activation and early mRNA turnover of brain
natriuretic peptide in cardiocyte hypertrophy: evidence for brain
natriuretic peptide as an emergency cardiac hormone against
ventricular overload. J Clin Invest 1995; 96: 12801287
6. Maeda K, Tsutamoto T, Wada A, Hisanaga T, Kinoshita M. Plasma
brain natriuretic peptide as a biochemical marker of high left
ventricular end-diastolic pressure in patients with symptomatic left
ventricular dysfunction. Am Heart J 1998; 135: 825832
7. Clerico A, Iervasi G, Del Chicca MG, Emdin M, Maffei S, Nannipieri M,
et al. Circulating levels of cardiac natriuretic peptides (ANP and BNP)
measured by highly sensitive and specific immunoradiometric assays
in normal subjects and in patients with different degrees of heart
failure. J Endocrinol Invest 1998; 21: 170179
8. Omland T, Aakvaag A, Bonarjee VV, Caidahl K, Lie RT, Nilsen DW, et
al. Plasma brain natriuretic peptide as an indicator of left ventricular
systolic function and long-term survival after acute myocardial
infarction. Comparison with plasma atrial natriuretic peptide and
IHJ-378-02.p65
39
15.
16.
17.
18.
19.
20.
21.
22.
5/6/2003, 9:59 AM
40 Baran et
al. IV Metoprolol in Patients with Positive ITTT
Original
Article
Background: Isoproterenol tilt-table testing provides a diagnosis of neurocardiogenic syncope in patients with
syncope or near-syncope. Although acute beta-blockade may prevent the development of syncope during
isoproterenol tilt-table testing, the use of beta-blockers for chronic prophylaxis may not be effective for some
patients who show a positive response to isoproterenol tilt-table testing. We evaluated whether the efficacy of
intravenous metoprolol in preventing symptoms during repeated tests would be helpful in selecting patients
suitable for long-term therapy.
Methods and Results: We studied 55 patients (35 females, 20 males; mean age 3611 years) who had been
chosen from a group referred to our institute with a history of unexplained syncope (>2 syncopal episodes) and
a positive response to isoproterenol tilt-table testing. After a positive response to isoproterenol tilt-table testing,
5 mg metoprolol was infused intravenously as a bolus and the test repeated. Thirty-five patients (group 1) showed
a positive response again and 20 (group II) showed a negative response. We started 50 mg metoprolol once a
day for patients in group 1 while group 2 was divided into 2 subgroups: the first subgroup (group 2a, 12 patients)
was started on 50 mg sertraline or 20 mg paroxetine once a day and the second subgroup (group 2b, 8 patients)
was started on 5 mg midodrine orally once a day. Two months later, isoproterenol tilt-table testing was repeated.
In group 1, 13 of 35 patients (37%) were positive on isoproterenol tilt-table testing while in group 2, 8 of 20
patients (40%) were positive on isoproterenol tilt-table testing (p not statistically significant). The therapies of
the two groups were then interchanged. Two months later (4 months from the beginning of the study), the
isoproterenol tilt-table test was repeated. Eleven patients in group 1 (31%) and 6 in group 2 (30%, p not
statistically significant) showed a positive response again.
Conclusions: We conclude that acute beta-blockade response to positive isoproterenol tilt-table testing is not a
useful predictor for the assessment of chronic prophylaxis for neurocardiogenic syncope. (Indian Heart J 2003;
55: 4043)
Key Words: Neurocardiogenic syncope, Tilt-table test, Beta-blockers
IHJ-368-02.p65
40
5/6/2003, 10:00 AM
Methods
Patients: We studied 89 patients (53 females and 36 males;
,
mean age 3816 years) who had been referred to our
institute with a history of unexplained syncope (>2
syncopal episodes). Cardiac and neurologic examination,
electrocardiogram, chest X-ray and echocardiogram were
normal in all the patients. Fifty-five patients (35 females,
20 males; mean age 3611 years) with a positive response
to ITTT (Table 1) formed the study group.
Around 1 week later, the ITTTs were repeated with
standard protocol and completed after an infusion of 5 mg
metoprolol (Table 2). Thirty-five patients (group 1) again
showed a positive response while 20 (group 2) showed a
negative response. We started patients in group 1 on 50
mg metoprolol once a day. Group 2 was divided into two
subgroups; the first subgroup: group 2a (12 patients) was
started on 50 mg sertraline or 20 mg paroxetine once a
day and the second subgroup: group 2b (8 patients) on 5
mg midodrine orally once a day. Two months later, the
ITTTs were repeated. During the ITTT, 3 patterns of
positive response were observed. A vasodepressor response
Table 1. Clinical characteristics of the study groups
Group 1 Group 2a Group 2b
Number of patients
35
Mean age (years)
3712
Women/men ratio
22/13
Syncopal episodes/year
5
Time to positive ITTT (seconds)
39
Baseline heart rate (bpm)
110
Baseline systolic BP (mmHg)
118
12
3410
7/5
4
47
106
121
8
3511
5/3
6
44
103
114
ITTT: isoproterenol tilt-table test; BP: blood pressure; bpm: beats per
minute; p value not statistically significant
Minutes
Tilt
Step I
Step II
Step III
Step III
Step III
0, 3, 5, 10 and 15
20, 25, 30, 35, 40 and 45
47 and 50
53
55,57 and 60
Step IV
Step IV
61 and 62
64, 66, 68 and 70
Systolic BP
Heart rate
ECG
Symptoms
Isoproterenol
Metoprolol
0
80
0
80
80
3 mcg/min
3 mcg/min
5 mcg/min
0
80
5 mcg/min
5 mcg/min
5 mg i.v.
IHJ-368-02.p65
41
5/6/2003, 10:00 AM
Discussion
IHJ-368-02.p65
42
5/6/2003, 10:00 AM
References
1. Brignole M, Alboni P, Benditt D, Bergfeldt L, Blanc JJ, Bloch Thomsen
PE, et al. Guidelines on management (diagnosis and treatment) of
syncope. Eur Heart J 2001; 22: 12561306
2. Boudoulas H, Nelson SD, Schaal SF, Lewis RP. Diagnosis and
management of syncope. In: Hursts the heart. 9th ed. McGraw-Hill;
1998. pp. 10591080
3. Perry JC, Garson A Jr. The child with recurrent syncope: autonomic
function testing and beta-adrenergic hypersensitivity. J Am Coll Cardiol
1991; 17: 11681171
4. OMarcaigh AS, MacLellan-Tobert SG, Porter CJ. Tilt-table testing and
oral metoprolol therapy in young patients with unexplained syncope.
Pediatrics 1994; 93: 278283
5. Raviele A, Brignole M, Sutton R, Alboni P, Giani P, Menozzi C, et al.
Effect of etilefrine in preventing syncopal recurrence in patients with
vasovagal syncope: a double-blind, randomized, placebo-controlled
trial. The Vasovagal Syncope International Study. Circulation 1999;
99: 14521457
6. Morillo CA, Leitch JW, Yee R, Klein GJ. A placebo-controlled trial of
intravenous and oral disopyramide for prevention of neurally
mediated syncope induced by head-up tilt. J Am Coll Cardiol 1993;
22: 18431848
7. Madrid AH, Ortega J, Rebollo JG, Manzano JG, Segovia JG, Sanchez A,
et al. Lack of efficacy of atenolol for the prevention of neurally
mediated syncope in a highly symptomatic population: a prospective,
double-blind, randomized and placebo-controlled study. J Am Coll
Cardiol 2001; 37: 554559
IHJ-368-02.p65
43
5/6/2003, 10:00 AM
44 Jadhav Article
et al. Endothelial Dysfunction and Prediction of
Original
CAD
Background: A noninvasive technique for testing endothelial function by ultrasound measurement of flowmediated dilatation has recently generated considerable interest as a marker of atherosclerosis, and in the
prediction of clinical coronary events and coronary artery disease.
Methods and Results: We measured the flow-mediated dilatation of the brachial artery (endotheliumdependent vasodilatation) in 136 subjects, with or without evidence of coronary artery disease. Endothelial
dysfunction was diagnosed if flow-mediated dilatation was less than 4.5%. Of the 136 subjects (age group
4070 years) recruited for the study, 94 were males and 42 females. Sixty-eight subjects had evidence of coronary
artery disease as diagnosed by documented hospitalization due to myocardial infarction or acute coronary
syndrome, proved by coronary angiography when feasible or noninvasive cardiac evaluation. Endothelial
dysfunction was detected in 90 subjects (66.2%). Prevalence of coronary artery disease was higher among
subjects with endothelial dysfunction compared to those without (57.5% v. 34.7%, p=0.013). Prevalence of
endothelial dysfunction was significantly higher among subjects with coronary artery disease as compared to
those without coronary artery disease (76.4% v. 55.8%, p=0.012). The present study showed a sensitivity of
76%, specificity of 44%, positive predictive value of 58% and negative predictive value of 65% for endothelial
dysfunction in the prediction of coronary artery disease. Multiple regression analysis using coronary artery
disease as a dependent variable revealed a statistically significant association with endothelial dysfunction
(p=0.033) even after the inclusion of traditional risk factors into the model.
Conclusions: We conclude that endothelial dysfunction shows a strong association with coronary artery disease
and can be a useful noninvasive tool for the evaluation of coronary artery disease. (Indian Heart J 2003; 55:
4448)
Key Words: Coronary artery disease, Endothelial dysfunction, Doppler ultrasound
IHJ-363-02.p65
44
5/6/2003, 10:01 AM
IHJ-363-02.p65
45
5/6/2003, 10:01 AM
+ HDL)
(Triglycerides
5
Parameters
CAD
(n=68)
Non-CAD
(n=68)
Age (years)
56.5311.47
48.7411
Male (%)
50 (53.1)
44 (46.8)
Smoking (%)
51 (75)
17 (25)
Hypertension (%)
21 (30.9)
30 (44.1)
Diabetes mellitus (%)
10 (14.7)
10 (14.7)
Body-mass index (kg/m2)
25.684.14
26.033.66
Fasting plasma glucose (mg/dl) 114.6141.92 114.1150.39
Total cholesterol (mg/dl)
194.9343.71 184.7338.66
LDL-cholesterol (mg/dl)
122.2641.29 111.1833.89
HDL-cholesterol (mg/dl)
40.935.80
41.73 6.10
Triglycerides (mg/dl)
155.0266.96 160.44107.70
CholesterolHDL ratio
4.791.11
4.520.92
Parameters
FMD
<4.5%
Age (years)
53.7311.67
Male (%)
67 (74.4)
Smoking (%)
71 (78.9)
Hypertension (%)
29 (32.2)
Diabetes mellitus (%)
15 (16.7)
Body-mass index (kg/m2)
25.483.89
Fasting plasma glucose (mg/dl) 118.749.1
Total cholesterol (mg/dl)
192.777.9
LDL-cholesterol (mg/dl)
120.039.7
HDL-cholesterol (mg/dl)
41.16.3
Triglycerides (mg/dl)
161.996.7
CholesterolHDL ratio
4.81.1
FMD
>4.5%
50.4812.06
27 (58.7)
42 (91.3)
22 (47.8)
5 (10.9)
26.613.85
106.039.1
141.766.8
110.934.5
41.75.4
150.074.8
4.40.8
IHJ-363-02.p65
46
p value
0.0001
0.265
0.012
0.374
0.374
0.602
0.951
0.270
0.110
0.457
0.754
0.157
p value
0.130
0.060
0.068
0.048
0.072
0.109
0.140
0.270
0.206
0.634
0.511
0.096
5/6/2003, 10:01 AM
17
(18.9)
11
(23.9)
28
(20.6)
Diabetes with
hypertension
29
(32.2)
22
(47.8)
51
(37.5)
29
(32.2)
8
(17.4)
37
(27.2)
FMD <4.5%
FMD >4.5%
Total
Without CAD
With CAD
Total
38
(55.9)
30
(44.1)
68
52
(76.5)
16
(23.5)
68
90
(66.2)
46
(33.8)
136
IHJ-363-02.p65
47
Sex
Age
Smoking
BMI >23 kg/m2
Cholesterol >180 mg/dl
LDL-c >130 mg/dl
HDL-c >40 mg/dl
Triglycerides >200 mg/dl
FMD (%) <4.5
Risk groups
p value
Odds ratio
0.934
0.019
0.198
1.000
0.555
0.624
0.539
0.560
0.033
0.173
1.047
1.053
2.411
1.000
1.473
1.395
0.717
1.390
0.321
0.723
Discussion
Ultrasonography is a reliable and accurate technique to
determine FMD in the superficial arteries. Reproduciblity
of FMD determination is best in the brachial artery in
healthy subjects and in patients with atherosclerosis.3,6
B-mode ultrasound scan including brachial artery FMD
may be of clinical value in the screening of patients with
CAD.6
In a study by Schroeder et al.,7 patients with CAD had a
significantly lower FMD% than patients without CAD. They
reported a sensitivity of 71%, a specificity of 81% with a
positive predictive value of 0.95 and a negative predictive
value of 0.41 for FMD in the prediction of CAD. They found
a better specificity and higher sensitivity for FMD as
compared to angina pectoris (sensitivity 95%, specificity
47.6%), exercise ECG (sensitivity 82.4%, specificity 57.1%),
and myocardial perfusion imaging (sensitivity 100%). The
present study showed a sensitivity of 76%, specificity of
44%, positive predictive value of 58%, and negative
predictive value of 65% for ED in the prediction of CAD.
The specificity and positive predictive value can be improved
by the selection of a healthy control group in the true sense,
inclusion of only coronary angiography-documented cases,
and utilizing automated tracking for the measurement of
arterial diameter.
In a study by Neunteufl et al.,8 impaired FMD in CAD
patients was related to the extent of CAD, to the maximum
percent diameter stenosis in one of the major coronary
vessels, brachial artery diameter, and plasma cholesterol
level on univariate analysis. On multiple regression
analysis, the extent of CAD (1-, 2- or 3-vessel disease) and
the baseline brachial artery diameter were independently
associated with FMD in CAD patients.8
5/6/2003, 10:01 AM
References
1. Raitakari OT, Celermajer DS. Flow-mediated dilatation. Br J Clin
Pharmacol 2000; 50: 397404
2. Celermajer DS. Testing endothelial function using ultrasound. J
Cardiovasc Pharmacol 1998; 32: 2932
3. Celermajer DS, Sorensen KE, Gooch VM, Spiegelhalter DJ, Miller OI,
Sullivan ID, et al. Non-invasive detection of endothelial dysfunction
in children and adults at risk of atherosclerosis. Lancet 1992; 340:
11111115
4. Celermajer DS, Sorensen KE, Georgakopoulos D, Bull C, Thomas O,
Robinson J, et al. Cigarette smoking is associated with dose-related
and potentially reversible impairment of endothelium-dependent
dilation in healthy young adults. Circulation 1993; 88: 21492155
5 Wendelhag I, Gustavsson T, Suurkula M, Berglund G, Wikstrand J.
Ultrasound measurement of wall thickness in the carotid artery:
fundamental principles and description of a computerized analysing
system. Clin Physiol 1991; 11: 565577
6. Sorensen KE, Celermajer DS, Spiegelhalter DJ, Georgakopoulus D,
Robinson J, Thomas O, et al. Non-invasive measurement of human
endothelium dependent arterial responses: accuracy and
reproducibility. Br Heart J 1995; 74: 247253
7. Schroeder S, Enderle MD, Ossen R, Meisner C, Baumbach A, Pfohl M,
et al. Noninvasive determination of endothelium-mediated
vasodilation as a screening test for coronary artery disease: pilot study
to assess the predictive value in comparison with angina pectoris,
exercise electrocardiography, and myocardial perfusion imaging. Am
Heart J 1999; 138: 731739
8. Neunteufl T, Katzenschlager R, Hassan A, Klaar U, Schwarzacher S,
Glogar D, et al. Systemic endothelial dysfunction is related to the extent
and severity of coronary artery disease. Atherosclerosis 1997; 129:
111118
9. Zhang X, Zhao SP, Li XP, Gao M, Zhou QC. Endothelium-dependent
and -independent functions are impaired in patients with coronary
heart disease. Atherosclerosis 2000; 149: 1924
10. Esper RJ, Vilarino J, Cacharron JL, Machado R, Ingino CA, Garcia
Guinazu CA, et al. Impaired endothelial function in patients with
rapidly stabilized unstable angina: assessment by noninvasive brachial
artery ultrasonography. Clin Cardiol 1999; 22: 699703
11. Suwaidi JA, Hamasaki S, Higano ST, Nishimura RA, Holmes DR Jr,
Lerman A. Long-term follow-up of patients with mild coronary artery
disease and endothelial dysfunction. Circulation 2000; 101: 948954
IHJ-363-02.p65
48
5/6/2003, 10:01 AM
Background: Supravalvar aortic stenosis is the rarest of left ventricular outflow obstructions. Data on this rare
entity from India are scarce.
Methods and Results: We retrospectively analyzed the data of 15 patients (13 males, mean age 15.510.18
years) with a diagnosis of supravalvar aortic stenosis confirmed by cardiac catheterization. Five patients had
morphological features of Williams syndrome. One patient had diffuse while the rest had discrete type of
supravalvar aortic stenosis. Five patients did not have any associated lesions. A 9-year-old male had an ascending
aortic aneurysm, and 3 patients had associated peripheral pulmonary artery stenosis. One child had a subaortic
ventricular septal defect, and another had severe mitral regurgitation. Twelve patients had electrocardiographic
evidence of left ventricular hypertrophy. Three patients had mild aortic valvar stenosis while 2 had aortic
regurgitation. Six patients had dilated coronary arteries. Two patients with supravalvar aortic gradients of 20
and 40 mmHg were kept on close follow-up. One patient was not willing to undergo surgery while the other is
awaiting surgery. Eleven patients underwent surgical correction. Dacron or pericardial patch aortoplasty was
done in all the patients. In addition, one patient each underwent pulmonary artery plasty, ventricular septal
defect closure, repair of ascending aortic aneurysm, and mitral valve replacement. The patient with diffuse type
of supravalvar aortic stenosis underwent augmentation aortoplasty. Two patients died perioperatively. One was
lost to follow-up. Two had moderate residual gradients. The rest of the patients were in New York Heart Association
functional class I on follow-up of 6.34.7 years.
Conclusions: Repair of supravalvar aortic stenosis by single sinus aortoplasty is safe and produces good results.
(Indian Heart J 2003; 55: 4954)
Key Words: Supravalvar aortic stenosis, Williams syndrome, Aortoplasty
IHJ-408-02.p65
49
5/6/2003, 10:01 AM
Age
(years)
Sex
Dysmorphism
Aortic valve
Associated cardiac
lesions
Coronaries
1
2
3
4
14
27
1.25
6
M
F
M
M
Nil
Nil
Nil
Nil
Nil
Valvular AS
MVP MR
Mild AR
Normal
Normal
NA
WS
WS
WS
Nil
Normal
Thickened, stenotic
Normal
Valve commissures fused
to ridge, NCC perforation
Normal
Thickened, stenotic
Normal
Normal
5
6
7
8
16
18
10
27
M
M
M
M
9
10
11
4.5
10
9
M
M
M
WS
Nil
Nil
Adherent LCC
Normal
Normal
12
13
14
15
15
26
10
34
F
M
M
M
Nil
Nil
WS
Nil
Normal
Adherent LCC
Normal
Adherent cusps, AR
Nil
VSD+valvular AS
RPA stenosis
Innominate artery
narrowing
Nil
Nil
Ascending aortic
aneurysm
LPA stenosis
Nil
LPA, RPA stenosis
Nil
Dilated
Normal
Normal
Normal
Dilated
Dilated, tortuous
Normal
Dilated
Normal
Dilated
Dilated, tortuous
Normal
WS: Williams syndrome; LCC: left coronary cusp; NCC: noncoronary cusp; AS: aortic stenosis; VSD: ventricular septal defect; AR: aortic regurgitation;
MVP: mitral valve prolapse; MR: mitral regurgitation; LPA: left pulmonary artery; RPA: right pulmonary artery; NA: data not available
IHJ-408-02.p65
50
5/6/2003, 10:01 AM
51
Age
(years)
Sex
Type
ECG
LV pressure
SV gradient
14
27
1.2
6
16
18
10
27
4.5
10
9
15
26
10
34
M
F
M
M
M
M
M
M
M
M
M
F
M
M
M
Diffuse
Localized
Localized
Localized
Localized
Localized
Localized
Localized
Localized
Localized
Localized
Localized
Localized
Localized
Localized
LVH strain
No LVH
LVH
No LVH
LVH
LVH
LVH
LVH
LVH
No LVH
LVH strain
LVH strain
LVH
LVH
LVH strain
230
120
154
190
120
250
170
340
200
150
302
300
200
205
170
150
20
90
70
56
70
76
215
122
40
200
180
80
100
50
Course/surgery
PA
Medical follow-up
PA+MVR
PA
PA
PA+VSD closure
PA+pulmonary arterioplasty
PA
PA
Medical follow-up
PA+aneurysmorrhaphy
PA
PA
Not willing for surgery
Awaiting surgery
PA: patch aortoplasty; LVH: left ventricular strain; MVR: mitral valve replacement; VSD: ventricular septal defect; SV: supravalvar
IHJ-408-02.p65
51
5/6/2003, 10:01 AM
IHJ-408-02.p65
52
5/6/2003, 10:01 AM
IHJ-408-02.p65
53
53
5/6/2003, 10:01 AM
IHJ-408-02.p65
54
5/6/2003, 10:01 AM
Background: Pulmonary arterial hypertension is a life-threatening disease for which continuous intravenous
infusion of prostacyclin has proved effective. However, it carries the risk of serious complications arising from
the complex delivery system. Prostacyclin analogs, endothelin antagonists, and the phosphodiesterase-5 inhibitor
sildenafil are emerging promising therapies. This study was aimed at evaluating the utility of oral sildenafil in
patients with pulmonary hypertension of varied etiology, poorly controlled on conventional treatment.
Methods and Results: Ten consecutive patients with pulmonary hypertension, either primary or related to
previous left-to-right shunts, thromboembolism, or interstitial lung disease, poorly controlled on conventional
therapy such as warfarin, calcium antagonists, digitalis, and diuretics, were included. A thorough clinical,
laboratory, and comprehensive echo Doppler evaluation was performed before enrollment in the trial to establish
the diagnosis and obtain baseline data. Subjects received sildenafil 25 mg 8 hourly, or a matching placebo for
two weeks each, in a randomized, double-blind, crossover design. A run-in period of two weeks was permitted
between the two therapies during which patients continued to receive the conventional therapy without any
vasodilator. At the end of each therapy period, the patients were evaluated for symptoms, New York Heart
Association class, distance covered during the 6 min walk test, rating of modified Borg dyspnea score, and
systolic pulmonary artery pressure using echo Doppler. The differences in the above variables at the end of
sildenafil and placebo therapies were compared. Nine patients completed the study protocol. Sildenafil, compared
to placebo, was associated with improved exercise tolerance as determined by the 6 min walk test
(266.67131.45 m v. 170105 m; p<0.005), decrease in modified Borg dyspnea score (3.561.01 v.
5.111.45; p<0.01), decrease in Doppler-estimated pulmonary artery systolic pressures (55.3316.52 mmHg
v. 75.3319.75 mmHg; p<0.005), improvement in New York Heart Association class (2 patients), and
improvement in symptoms. Sildenafil was well tolerated with no untoward effects; further, no significant changes
in heart rate or blood pressure occurred during the study period.
Conclusions: Sildenafil improves exercise capacity and symptoms, and decreases pulmonary artery pressures
in patients with primary or secondary pulmonary hypertension of varied etiology. (Indian Heart J 2003; 55:
5559)
Key Words: Pulmonary hypertension, Sildenafil, Echocardiography
IHJ-395-02.p65
55
5/6/2003, 10:02 AM
Methods
Selection of patients: Ten consecutive, symptomatic
(NYHA class >II) patients with Doppler-estimated
pulmonary systolic pressure >35 mmHg with normal left
ventricular function and no reversible cause for PAH were
taken up for the study. They gave well-informed written
consent for participation in the study and all except one
completed the study protocol. The institutional ethics
committee approved the protocol. Patients were excluded
if they had any contraindications to sildenafil therapy or if
they had any reversible cause for pulmonary hypertension
such as valvular heart disease.
Study design: The study was carried out at a large referral
center of central India as a prospective, randomized,
double-blind, crossover trial. To establish the diagnosis,
patients were subjected to a thorough physical
examination, routine laboratory evaluation, chest X-ray,
electrocardiogram (ECG), and comprehensive echocardiographic evaluation at baseline. Before randomization, they
were allowed a run-in period of one week after stoppage of
their previous vasodilator therapy; they then received either
sildenafil 25 mg 8 hourly or matching placebo for two
weeks in a crossover design with a washout period of at
least two weeks between the two therapies.
Outcome measures: The patients were evaluated for
exercise capacity as indicated by the 6 min walking
distance. The secondary measures of efficacy were change
in symptoms and NHYA functional class, change in
modified Borg dyspnea index10 (a measure of perceived
breathlessness on a scale of 0 to 10, with higher values
indicating more severe dyspnea), and change in resting
pulmonary artery systolic pressures as estimated from
Doppler tricuspid regurgitant jet velocities or from the
gradient across the ventricular septal defect or patent
IHJ-395-02.p65
56
Patients (n)
1860 years
Mean 32.11 years, SD 15.06 years
Male
Female
4
5
II
III
IV
3
5
1
II
III
IV
4
5
0
Post-sildenafil
therapy
Diagnosis
Primary pulmonary hypertension
Pulmonary hypertension associated with:
Interstitial lung disease
Thromboembolism
Eisenmenger syndrome
Ventricular septal defect
Patent ductus arteriosus
Treatment at inclusion
Warfarin
Nifedipine
Frusemide
Spironolactone
Digoxin
5/6/2003, 10:02 AM
3
2
1
2
1
9
4
2
2
2
Baseline
Placebo Sildenafil
163.89
110.73
170
105
266.67
131.45
5.98
<0.005
5.22
1.64
5.11
1.45
3.56
1.01
3.56
<0.01
80.78
21.30
75.33
19.75
55.33
16.52
4.33
<0.005
IHJ-395-02.p65
57
Fig. 1. Mean change from baseline at week 8 in results of the (A) 6 minute
walk test, (B) modified Borg dyspnea index, and (C) pulmonary artery systolic
pressure in patients while on sildenafil and placebo. Numbers indicate the mean
values. Standard error of the mean is given in parentheses.
5/6/2003, 10:02 AM
IHJ-395-02.p65
58
5/6/2003, 10:02 AM
IHJ-395-02.p65
59
5/6/2003, 10:02 AM
60 Puri et Article
al. Polymorphism in the Apo B-100 Gene
Original
Background: The aim of this study was to investigate the association of apolipoprotein B gene polymorphisms
with coronary artery disease and lipid levels in Indians.
Methods and Results: One hundred patients of angiographically proven atherosclerotic coronary artery disease
and one hundred age- and sex-matched control subjects (treadmill negative) were included in the study. Serum
lipids including cholesterol, triglycerides, high-density lipoprotein, low-density lipoprotein, very low-density
lipoprotein, and apolipoprotein B were analyzed. Genomic DNA was extracted and the apolipoprotein B 3'
hypervariable region amplified by polymerase chain reaction. Regions carrying Xba1, EcoR1, and Msp1
restriction sites present in the apolipoprotein B gene were amplified and digested separately by the respective
enzymes. Restriction fragment length polymorphism analysis showed that EcoR1 with the R+/R+ genotype was
significantly more common in patients with coronary artery disease. Overall, the genotypes EcoR1+/+, Msp1+/+,
Xba1+/+ and Eco R1+/+ Msp1+/, Xba1/ were significantly more common in patients as compared to controls
(p<0.05). When gene polymorphisms were compared with lipid abnormalities, the genotypes
EcoR1+/+, Xba1/, and Msp1+/+ were more frequent in patients with elevated apolipoprotein B and very
low-density lipoprotein levels. On the other hand, these genotypes were less common in patients with increased
total cholesterol and low-density lipoprotein levels. When we studied the individual alleles of the variable number
of tandem repeats region, we observed that allele 34 was significantly increased in patients with coronary
artery disease as compared to controls. Allele 36 was present with a frequency of 1% in controls while it was
totally absent in patients.
Conclusions: This study identifies the apolipoprotein B gene polymorphism associated with coronary artery
disease. An association between apolipoprotein B gene polymorphisms and elevated apolipoprotein B and very
low-density lipoprotein levels was observed. However, there was no positive association with other elevated lipid
levels in North Indians from Uttar Pradesh. (Indian Heart J 2003; 55: 6064)
Key Words: Apolipoprotein B, Polymorphism, Coronary artery disease
IHJ-417-02.p65
60
5/6/2003, 10:03 AM
Methods
Subjects: One hundred patients of angiographically
proven CAD evaluated at the Cardiology Department of the
Sanjay Gandhi Postgraduate Institute of Medical Sciences,
Lucknow, Uttar Pradesh, India were included in the study.
Patients less than 6 weeks post-myocardial infarction (MI)
were excluded from the study. One hundred age- and sexmatched controls were also selected for the study. The
controls were subjected to a treadmill test to ensure that
they were not suffering from any CAD. Further, all controls
with hypertension, diabetes, and endocrine or metabolic
disorders were excluded. Informed consent was taken from
both the patients and controls.
61
5
349 bp
239 bp
110 bp
675 bp
Lane 1: 25 bp ladder
Lane 2 and 4: Undigested samples
Lane 3 and 5: Digested sample (+/+)
415 bp
35 bp
33 bp
31 bp
260 bp
Fig. 1. Apo B-gene polymorphism. A: Apo B 3' VNTR analysis; B: Msp1 RFLP analysis; C: Xba1 RFLP analysis; D: EcoR1 RFLP analysis
IHJ-417-02.p65
61
5/6/2003, 10:03 AM
Controls (n=100)
0.950
0.050
0.285
0.715
0.825
0.175
0.820
0.180
0.225
0.775
0.850
0.150
8
91
34*
65*
Genotypes *
E+ E+ M+ M+ X+ X+
E+ E+ M+ M X X
E+ E M+ M X X
10
20
1
2**
8**
9**
Allele frequency
EcoR1 (+)
EcoR1 ()
Xba1 (+)
Xba1 ()
Msp1 (+)
Msp1 ()
IHJ-417-02.p65
62
Fig. 2. Apo B 3' VNTR allele frequency distribution among patients with CAD
and controls.
5/6/2003, 10:03 AM
Discussion
On the basis of evidence obtained over many years from
epidemiological and trial data, LDL- and HDL-cholesterol
levels have been the recommended lipid variables in
international guidelines for treatment. However, new
information shows the importance of apo B and apo A-I as
risk predictors for CAD.16 A reason why apo B may be a
stronger predictor of risk than LDL-cholesterol is that apo B
is present not only in LDL but also in VLDL, intermediate
density lipoprotein, and lipoprotein (a). Therefore, the sum
of apo B concentrations in all atherogenic particles might
be a better risk marker than total cholesterol and LDLcholesterol levels only.16 In our study, the entire lipid levels,
including those of apo B, were higher in patients as
compared to controls; however, these did not reach
statistical significance. One possible explanation for this
could be that lipid-lowering drugs were not withheld prior
to lipid testing for this study as this would not have been
ethically justifiable in patients who had angiographically
proven CAD with dyslipidemia and were already on lipidlowering drugs.
It has been suggested that in addition to quantitative
variation in apo B levels in the plasma, genetic variation at
the apo B locus may be a new and independent risk factor
for CAD.17
It has been reported that different VNTR alleles may be
associated with CAD and hyperlipidemia.46 We found an
association of VNTR 34 in patients with CAD similar to
that reported by Moreel et al.4 The allelic variation of apo B
gene polymorphisms may have some association with
various ethnic groups. Deka et al.9 in a study of allelic
frequency distribution at the hypervariable locus 3' to the
apo B gene in 5 human populations found 12 segregating
alleles in 319 individuals. They found that the two most
frequent alleles, 37 and 39, were present in all the
populations. When we studied VNTR we found that allele
34 was significantly increased in patients as compared to
controls, while allele 36 was completely absent in patients
but present in controls. This clearly demonstrates the
presence of allelic frequency variation in different
populations. These association studies may be of some use
when genetic factors are considered as one of the
predisposing causes.
There are few studies on Indians that show the
association of the apo B gene 3' HVR alleles with CAD and
plasma lipid levels. Renges et al.18 found an association
between Xba1 and ins/del polymorphisms of the apo B gene
with total cholesterol and HDL-cholesterol levels in South
Asians in the UK. Saha et al. 19 reported that DNA
polymorphisms of the apo B gene were associated with
IHJ-417-02.p65
63
63
5/6/2003, 10:03 AM
IHJ-417-02.p65
64
5/6/2003, 10:03 AM
Two cases of isolation of the left subclavian artery from the aortic arch are reported for the rarity of this lesion.
One patient was diagnosed clinically, the other after angiography. The isolated left subclavian artery was
reimplanted in one patient. This rare anomaly has clinical and surgical relevance and should be diagnosed by
diligent clinical and angiographic evaluation. (Indian Heart J 2003; 55: 6567)
Key Words: Isolated left subclavian artery, Subclavian steal, Arch anomalies
Case Report
Case 1: A two-year-old child presented to us with a history
of mild cyanosis since 6 months of age and a history of
one episode of a cyanotic spell one month ago. On
examination he had mild cyanosis and clubbing. The left
arm pulse was weaker compared to the right arm. The blood
pressure was 70/40 mmHg in the left arm and 104/60
mmHg in the right arm. Cardiovascular examination
revealed a quiet precordium, single second heart sound, and
a grade III/VI ejection systolic murmur in the left
parasternal area. Chest X-ray showed a right aortic arch,
no cardiomegaly and oligemic lung fields. An
electrocardiogram (ECG) showed right axis deviation with
right ventricular hypertrophy. Typical anatomy of the
tetralogy of Fallot (TOF) was seen on echocardiogram. In
view of TOF, right aortic arch and weak left arm pulse,
isolation of the LSA was suspected. Subsequent
catheterization confirmed the presence of TOF with
confluent and good-sized pulmonary arteries. Aortogram
revealed a right aortic arch. The innominate, right and left
common carotid arteries were normal. On aortography, the
LSA did not show any opacification (Fig. 1). Late frames
showed faint opacification of the LSA by retrograde filling
Correspondence: Dr Shyam S Kothari, Department of Cardiology,
Cardiothoracic Centre, All India Institute of Medical Sciences, New Delhi
110029. e-mail: kotharis@del2.vsnl.net.in
IHJ-386-02.p65
65
Fig. 1. Arch aortogram showing the branches of the aortic arch with failure of
opacification of the left subclavian artery.
5/6/2003, 10:03 AM
Fig. 2. Late frames of the same injection as in Fig.1 show retrograde filling of
the left vertebral artery (white arrow) which supplies the left subclavian artery
(black arrow).
mmHg in the right arm and 82/60 mmHg in the left arm.
The arterial saturation by oximetry was 85% in room air
in all four limbs. Cardiovascular examination revealed
cardiomegaly, single second heart sound, left ventricular
third heart sound, and a pansystolic murmur at the apex.
ECG showed left axis deviation with a counterclockwise loop
and right ventricular hypertrophy. Chest X-ray revealed
cardiomegaly, a right aortic arch, and increased pulmonary
blood flow. Echocardiography showed atrioventricular
septal defect (AVSD) and a double outlet right ventricle
(DORV) with dilated left ventricle and atrium. The great
vessels were malposed with an anterior aorta. There was
no pulmonic stenosis. Cardiac catheterization and
aortography were performed. The aortogram revealed a
right aortic arch with absence of filling of the LSA from
the aorta (Fig. 3) and delayed retrograde filling from the
left vertebral artery. A selective left common carotid
angiogram showed retrograde filling of the LSA through
the left vertebral artery (Fig. 4). Right ventricular
angiogram confirmed the presence of a DORV. Hence, a
diagnosis of cyanotic congenital heart disease with DORV,
AVSD, and isolated LSA was made. The child subsequently
developed lower respiratory tract infection and succumbed
to it.
Discussion
Isolation of the LSA is defined as a loss of continuity
between the LSA and the aorta with a persistent connection
to the homolateral pulmonary artery through the ductus
IHJ-386-02.p65
66
Fig. 3. Arch aortogram showing opacification of the branches of the aortic arch.
Note the absence of opacification of the left subclavian artery.
Fig. 4. Late frames from selective left common carotid angiogram showing
retrograde filling of the left vertebral artery (arrowhead) and the left subclavian
artery (black arrow).
5/6/2003, 10:03 AM
IHJ-386-02.p65
67
5/6/2003, 10:03 AM
68 Pandurangi
Brief
Report et al.
Endoepicardial AV Pacing
Complete heart block following intracardiac surgical repair for complex congenital heart disease is not
uncommon. In the presence of ventricular dysfunction, ventricular pacing alone may not improve the cardiac
output. We report the feasibility and efficacy of endoepicardial atrioventricular sequential pacing in a case of
postoperative complete heart block. (Indian Heart J 2003; 55: 6870)
Key Words: Complete heart block, Atrioventricular sequential pacing, Cardiac surgery
Case Report
A 12-year-old girl had undergone surgical closure for atrial
and ventricular septal defects, with subpulmonic resection
at 6 years of age for situs inversus, dextrocardia, atrial and
ventricular septal defects, corrected transposition of the
great arteries (c-TGA), subpulmonic stenosis and
interrupted inferior vena cava. The patient underwent a
Correspondence: Dr Ulhas M Pandurangi, Department of Cardiology,
Institute of Cardiovascular Diseases, Madras Medical Mission, 4-A,
Dr J Jayalalitha Nagar, Mogappair, Chennai 600050.
e-mail: ulhaspandurangi@hotmail.com
IHJ-392-02.p65
68
5/6/2003, 10:04 AM
Fig. 3. Fluoroscopy (PA view) showing endocardial atrial lead (single arrow)
and epicardial ventricular lead (double arrow).
IHJ-392-02.p65
69
69
5/6/2003, 10:04 AM
IHJ-392-02.p65
70
6. Romero LR, Haffajee CI, Levin W, Doherty PW, Berkovits BV, Alpert
JS. Non-invasive evaluation of ventricular function and volumes
during atrioventricular sequential and ventricular pacing. Pacing Clin
Electrophysiol 1984; 7: 1017
7. Doty DB, Truesdell SC, Marvin WJ Jr. Techniques to avoid injury of
the conduction tissue during the surgical treatment of corrected
transposition. Circulation 1983; 68: II6369
8. Fitzpatrick A, Sutton R. A guide to temporary pacing. BMJ 1992; 304:
365369
9. Waldo AL, MacLean WAH. Diagnosis and treatment of cardiac
arrhythmias following open heart surgery. 2nd ed. Mt Kisco, New York:
Futura; 1980. p. 64
10. Moungey SJ. Temporary A-V sequential pacemakers. Programming
and troubleshooting. Prog Cardiovasc Nurs 1989; 4: 4960
11. Haywood DL. Temporary A-V sequential pacing using an epicardial
lead system. Crit Care Nurse 1985; 5: 2124
12. Roth JV, Huertas R. Atrioventricular sequential pacing using
transesophageal atrial pacing in combination with a temporary DDD
pacemaker for atrial tracking and ventricular pacing. J Cardiothorac
Vasc Anesth 1995; 9: 255258
13. Roth JV. Temporary transmyocardial pacing using epicardial pacing
wires and pacing pulmonary artery catheters. J Cardiothorac Vasc
Anesth 1992; 6: 663667
5/6/2003, 10:04 AM
We describe a patient who underwent percutaneous coronary intervention combined with bilateral iliac and
left renal artery angioplasty during the same sitting. Stenting of the coronary and peripheral arteries was
performed employing the direct stenting technique. No complications occurred. The patient was discharged
2 days after the intervention and remains asymptomatic, leading a fully active life during 1 year of follow-up. To
our knowledge, unstaged coronary stenting combined with direct stenting of the renal and both common iliac
arteries has not been reported previously in India. (Indian Heart J 2003; 55: 7174)
Key Words: Coronary artery disease, Peripheral vascular disease, Stenting
Case Report
IHJ-348-02.p65
71
5/6/2003, 10:04 AM
b
Fig. 1. Left anterior descending coronary artery stenosis before (a) and after
(b) stenting.
IHJ-348-02.p65
ostial location of the lesion and the acute angle of the aortic
bifurcation. After cannulating the right femoral vein with
a 0.38" guidewire, the right femoral artery was punctured
under fluoroscopic guidance. This was done because the
right femoral artery pulsation was very feeble and difficult
to localize. A 7 F sheath was inserted into the right femoral
artery and a retrograde angiogram through the sheath
delineated the tight stenosis of the right common iliac
artery. A peak pressure gradient of 80 mmHg on pull-back
was recorded across the lesion. The lesion was crossed with
a 0.014" balance middle weight coronary guidewire and
exchanged for a 0.035" Amplatz super stiffTM (Boston
Scientific) guidewire. A CorinthianTM stent (Cordis) 17 mm
72
Fig. 2. Right and left common iliac artery stenosis before (a) and after (b)
stenting.
5/6/2003, 10:04 AM
73
IHJ-348-02.p65
73
b
Fig. 3. Left renal artery stenosis before (a) and after (b) stenting.
5/6/2003, 10:04 AM
IHJ-348-02.p65
74
5. Hertzer NR, Young JR, Beven EG, OHara PJ, Graor RA, Ruschhaupt
WF, et al. Late results of coronary bypass in patients with peripheral
vascular disease. I. Five-year survival according to age and clinical
cardiac status. Cleve Clin Q 1986; 53: 133143
6. Hertzer NR, Young JR, Beven EG, OHara PJ, Graor RA, Ruschhaupt
WF, et al. Late results of coronary bypass in patients with peripheral
vascular disease. II. Five-year survival according to sex, hypertension,
and diabetes. Cleve Clin J Med 1987; 54: 1523
7. Crawford ES, Bomberger RA, Glaeser DH, Saleh SA, Russell WL.
Aortoiliac occlusive disease: factors influencing survival and function
following reconstructive operation over a twenty-five-year period.
Surgery 1981; 90: 10551067
8. Sigwart U, Puel J, Mirkovitch V, et al. Intravascular stents to prevent
occlusion and restenosis after transluminal angioplasty. N Engl J Med
1991; 316: 1317
9. Serruys PW, de Jaegere P, Kiemeneij F, Macaya C, Rutsch W,
Heyndrickx G, et al. A comparison of balloon-expandable-stent
implantation with balloon angioplasty in patients with coronary
artery disease. Benestent Study Group. N Engl J Med 1994; 331: 489
495
10. Figulla HR, Mudra H, Reifart N, Werner GS. Direct coronary stenting
without predilatation: a new therapeutic approach with a special
balloon catheter design. Cathet Cardiovasc Diagn 1998; 43: 245252
11. Carrie D, Khalife K, Citron B, Izaaz K, Hamon M, Juiliard JM, et al.
Comparison of direct coronary stenting with and without balloon
predilatation in patients with stable angina pectoris. BET (Benefit
Evaluation of Direct Coronary Stenting) Study Group. Am J Cardiol
2001; 87: 693698
12. Wilson SH, Berger PB, Mathew V, Bell MR, Garratt KN, Rihal CS, et al.
Immediate and late outcomes after direct stent implantation without
balloon predilation. J Am Coll Cardiol 2000; 35: 937943
13. Veselka J, Mates M, Tesar DB, Aschermann M, Urbanova T, Honek T.
Direct stenting without predilatation: a new approach to coronary
intervention. Coron Artery Dis 2000; 11: 503507
14. Dorros G, Mathiak L. Direct deployment of the iliofemoral balloon
expandable (Palmaz) stent utilizing a small (7.5 French) arterial
puncture. Cathet Cardiovasc Diagn 1993; 28: 8082
15. Mehan VK, Meier B. Multiple renal artery stenting with half
(disarticulated) PalmazSchatz coronary stents and simultaneous
coronary angioplasty. Indian Heart J 1995; 47: 259260
5/6/2003, 10:04 AM
Catheter ablation for atrial tachycardia is limited by its low success rate and prolonged procedure time because
of difficulties in mapping the site of the tachycardia. A new three-dimensional mapping system, the Cardiac
Pathways mapping system, using an ultrasound transducer, has recently become available. We report a case of
focal atrial tachycardia ablation with this system. (Indian Heart J 2003; 55: 7577)
Key Words: Ablation, Tachyarrhythmia, Cardiac mapping
IHJ-364-02.p65
75
5/6/2003, 10:05 AM
b
Fig. 2. Isochrone mapping of the right and left atrium on the Cardiac Pathways
system showing the earliest activation site in the roof of the left atrium.
LAO 40o (a) and RAO 30o (b). The right panel of the pictures shows the
earliest activation signal in the ablation catheter (68 ms early from the
reference catheter). CS: coronary sinus; RV: right ventricle; ABL: ablation
catheter
IHJ-364-02.p65
76
5/6/2003, 10:05 AM
IHJ-364-02.p65
77
5/6/2003, 10:05 AM
78 Kothari
et al.
Brief
Report
A 45-day-old infant presented with the unusual and intriguing symptom of episodic crying and loss of
consciousness. The infant was discovered to have a vascular compression of the trachea by the innominate
artery, almost serendipitously. He was cured of his symptoms by anterior suspension of the innominate artery.
(Indian Heart J 2003; 55: 7880)
Key Words: Vascular ring, Apnea, Aortopexy
IHJ-441-03.p65
78
5/6/2003, 10:05 AM
IHJ-441-03.p65
79
5/6/2003, 10:05 AM
IHJ-441-03.p65
80
5/6/2003, 10:05 AM
IHJ-365-02.p65
81
5/6/2003, 10:05 AM
Year
Drug
No. of
patients
Protocol
End-point
Relative
benefits
ERA7
REDUCE8
FACT9
ENTICES10
1994
1996
1997
1998
Enoxaparin
Reviparin
Nadroparin
Enoxaparin
458
612
354
123
R, C, B
R, PC, B
R, PC, B
R, C
2% (p=ns)
4% (p=ns)
6% (p=ns)
25%
LMWH: low-molecular-weight heparin; PTCA: percutaneous transluminal coronary angioplasty; R: randomized; B: blinded; C: controlled; PC: placebocontrolled; ns: statistically not significant
*No further heparin of any type was administered after the procedure and vascular access sheaths were removed 4 hours after the enoxaparin bolus
PCI: percutaneous coronary intervention; MI: myocardial infarction
IHJ-365-02.p65
82
Fig. 1. Major bleeding incidence with or without events related to CABG and
transfusion requirements up to 30 days post-PCI in the NICE 1 and NICE 4
trials.
5/6/2003, 10:05 AM
Fig. 3. Major and minor bleeding with and without CABG and requirement for
blood product transfusion in the NICE 1 trial versus the EPISTENT stent plus
placebo cohort; events up to 30 days.
IHJ-365-02.p65
83
5/6/2003, 10:05 AM
IHJ-365-02.p65
84
(%)
0.3
3.4
2.1
5.7
27.9
4.5
25
10.5
1.9
5/6/2003, 10:05 AM
Table 4. Overview of Enoxaparin and Ticlopidine after Elective Stenting (ENTICES) study
Inclusion criteria of patients
Multicenter, randomized
Treatment regimen
Pre-procedure
Control
Enoxaparin
UFH/warfarin, aspirin 325 mg/day,
Aspirin 325 mg/day,
dipyridamole 75 mg 3 times daily,
ticlopidine 250 mg twice
dextran 100 mg/hour
daily, dipyridamole
Dextran and UFH to maintain ACT
UFH to maintain ACT
at 300350 s
of 300350 s
UFH 2500 U IV bolus 6 hours after
Enoxaparin 3060 mg
sheath removal, then infusion until
subcutaneously twice
prothrombin time 5070 s, dextran
daily for 10 days,
until 2 hours after restarting UFH.
*ticlopidine 250 mg twice
Aspirin, dipyridamole, and warfarin
daily for 1 month
(INR 2.03.0) for 30 days
Death, MI, stent thrombosis, bypass surgery (CABG), and repeat PTCA at 30 days, individually
and the composite of all clinical events, in-hospital hemorrhagic complications
Procedure
Post-procedure
Clinical end-points
Results (%)
Control (n=44)
Enoxaparin (n=79)
p value
5
11
7
9
7
20
16
0
4
0
0
1
5
5
0.13
0.13
0.04
0.02
0.13
0.01
0.05
Death
MI
Stent thrombosis
Bypass surgery
Repeat PTCA
Composite
Hemorrhagic/vascular complications
* The enoxaparin dose was 30 mg, 40 mg or 60 mg in patients weighing <70 kg, 70100 kg and >100 kg, respectively.
UFH: unfractionated heparin; IV: intravenous; ACT: activated clotting time; INR: international normalized ratio; PTCA: percutaneous transluminal coronary
angioplasty
IHJ-365-02.p65
85
5/6/2003, 10:05 AM
IHJ-365-02.p65
86
5/6/2003, 10:05 AM
4.
5.
6.
7.
8.
9.
10.
11.
IHJ-365-02.p65
87
5/6/2003, 10:05 AM
88
Shrivastava
Point
of Viewet al. Echocardiographic Anatomy of Atrial Septal Defect
Fig. 3. Atrioventricular (AV) and atrial rims on (a) transthoracic echocardiography in the subcostal coronal view, and (b) on transesophageal echocardiography in the 4-chamber view.
Fig. 2. Superior vena caval (SVC) and inferior vena caval (IVC) rims on (a)
transthoracic echocardiography in the subcostal sagittal view, and (b) on
transesophageal echocardiography in the basal long-axis view.
IHJ-366-02.p65
88
5/6/2003, 10:06 AM
IHJ-366-02.p65
89
89
References
1. Reddy SCB, Rao PS, Evenko J, Koscik R, Wilson AD. Echocardiographic predictors of success of catheter closure of atrial septal defect
with the buttoned device. Am Heart J 1995; 129: 7686
2. Rosenfeld HM, Velde MEV, Sanders SP, Colan SD, Parness IA, Lock
JE, et al. Echocardiographic predictors of candidacy for successful
transcatheter atrial septal defect closure. Cathet Cardiovasc Diagn
1995; 34: 2934
3. Magni G, Hijazi ZM, Pandian NG, Delabays A, Sugeng L, Laskari C,
et al. Two-dimensional and three-dimensional transesophageal
echocardiography in patient selection and assessment of atrial septal
defect closure by the new DAS-Angel Wings Device: initial clinical
experience. Circulation 1997; 96: 17221728
5/6/2003, 10:06 AM
90 Anandaraja et al.
Migration of
Cardiovascular
Images
Fig. 1. Right anterior oblique view (a) and left anterior oblique view (b) showing migrated pacemaker lead in the coronary sinus (arrow). Also visible is a proximally
severed unipolar lead (white arrowhead), and another detached pacemaker lead lying freely within the right atrium (bold arrow). The white arrow indicates the new
pacemaker lead.
IHJ-Images.p65
90
5/6/2003, 10:07 AM
IHJ-Images.p65
91
5/6/2003, 10:07 AM
Letters
to to
the
92 Letters
theEditor
Editor
Letter-to-Editors.p65
92
5/6/2003, 10:07 AM
References
1. Sengupta PP, Mohan JC, Pandian NG. Tissue Doppler
echocardiography: principles and applications. Indian Heart J 2002;
54: 368378
2. Maslak SH, Freund JG. Color Doppler instrumentation. In: Lanzer P
(ed). Vascular imaging by color Doppler and magnetic resonance. Berlin,
Heidelberg: Springer-Verlag; 1991. pp.87123
George Thomas
Department of Cardiology
Indira Gandhi Co-operative Hospital, Kochi
Reply
Letter-to-Editors.p65
93
5/6/2003, 10:07 AM
5.
6.
7.
8.
Letter-to-Editors.p65
94
References
1. Waggoner AD, Bierig SM. Tissue Doppler imaging: a useful
echocardiographic method for the cardiac sonographer to assess
systolic and diastolic ventricular function. J Am Soc Echocardiogr 2001;
14: 11431152
2. Pislaru C, Abraham TP, Belohlavek M. Strain and strain rate
echocardiography. Curr Opin Cardiol. 2002; 17: 443454
3. Evans DH, McDicken WN. Doppler ultrasound physics, instrumentation
and signal processing, 2nd ed. West Sussex: John Wiley and Sons; 2000.
pp. 526
4. Evans DH, McDicken WN. Doppler ultrasound physics, instrumentation
and signal processing. 2nd ed. West Sussex: John Wiley and Sons; 2000.
pp. 345347
5. Gorcsan J 3rd, Strum DP, Mandarino WA, Gulati VK, Pinsky MR.
Quantitative assessment of alterations in regional left ventricular
contractility with color-coded tissue Doppler echocardiography.
Comparison with sonomicrometry and pressurevolume relations.
Circulation 1997; 95: 24232433
6. Anderson T, McDicken WN. Measurement of tissue motion. Proc Inst
Mech Eng [H] 1999; 213: 181191
7. Fathi R, Cain P, Nakatani S, Yu HC, Marwick TH. Effect of tissue
Doppler on the accuracy of novice and expert interpreters of
dobutamine echocardiography. Am J Cardiol 2001; 88: 400405
8. Edvardsen T, Gerber BL, Garot J Bluemke DA, Lima JA, Smiseth OA.
Quantitative assessment of intrinsic regional myocardial deformation
by Doppler strain rate echocardiography in humans: validation
against three-dimensional tagged magnetic resonance imaging.
Circulation 2002; 106: 5056
9. Frommelt PC, Ballweg JA, Whitstone BN, Frommelt MA. Usefulness
of Doppler tissue imaging analysis of tricuspid annular motion for
determination of right ventricular function in normal infants and
children. Am J Cardiol 2002; 89: 610613
10. Sogaard P, Egeblad H, Pedersen AK, Kim WY, Kristensen BO, Hansen
PS, et al. Sequential versus simultaneous biventricular
resynchronization for severe heart failure: evaluation by tissue
Doppler imaging. Circulation 2002; 106: 20782084
5/6/2003, 10:07 AM
Letter-to-Editors.p65
95
5/6/2003, 10:07 AM
Letter-to-Editors.p65
96
19.
20.
21.
22.
Panagiotis Korantzopoulos
Laboratory of Biological Chemistry, University of
Ioannina Medical School, Ioannina, Greece
Dimitrios Papaioannides
Department of Medicine
Arta General District Hospital
Arta, Greece
5/6/2003, 10:07 AM
Selected Summaries
97
Selected
Summaries
Comments
IHJ-Selected Summary.p65
97
5/6/2003, 10:08 AM
98
Selected Summaries
Major Outcomes in High-Risk Hypertensive Patients Randomized to AngiotensinConverting Enzyme Inhibitor or Calcium-Channel Blocker v. Diuretics
The ALLHAT Collaborative Research Group. JAMA 2002; 288: 29812997
Summary
The Antihypertensive and Lipid-Lowering Treatment to
Prevent Heart Attack Trial (ALLHAT) was a randomized,
double-blind, active controlled, clinical trial conducted with
a view to determine which antihypertensive treatment
decreased the risk of coronary artery disease (CAD) or other
cardiovascular disease (CVD) events. It enrolled 33 357
hypertensive subjects, both men and women, >55 years of
age, with at least one other risk factor for CAD from 623
North American centers. The patients were randomized to
receive chlorthalidone 12.525 mg/day (n=15 255),
amlodipine 2.510 mg/day (n=9048), or lisinopril 1040
mg/day (n=9054), and followed up for 8 years. The primary
end-point was a combination of CAD deaths plus nonfatal
myocardial infarction (MI). The secondary end-points were
all-cause mortality, stroke, combined CAD end-point (CAD
death, nonfatal MI, coronary revascularization, or angina
requiring hospitalization), and combined CVD (combined
CAD end-point, stroke, treated angina without
hospitalization, CHF and peripheral arterial disease). At a
mean follow-up of 4.9 years, the primary outcome of CAD
death plus nonfatal MI was not different in any of the
treatment groups. Compared with chlorthalidone (6-year
rate, 11.5%), the relative risks (RRs) were 0.98 (95% CI:
0.901.07) for amlodipine (6-year rate, 11.3%) and 0.99
(95% CI: 0.911.08) for lisinopril (6-year rate, 11.4%).
Similarly, all-cause mortality was also not different.
Chlorthalidone was more effective in controlling systolic
BP as compared to amlodipine and lisinopril (p<0.05 for
both). On the other hand, amlodipine was more effective
in lowering the diastolic BP (p<0.01). Among the
secondary end-points, occurrence of CHF was commoner
in the amlodipine group as compared to the chlorthalidone
group (10.2% v. 7.7%, RR 1.38; 95% CI: 1.251.52).
Similarly, combined CAD end-points (33.3% v. 30.9%, RR
1.10; 95% CI: 1.051.16), stroke (6.3% v. 5.6%, RR 1.15;
95% CI: 1.021.30), and CHF (8.7% v. 7.5%, RR 1.19; 95%
CI: 1.071.31) were all higher in the lisinopril group
compared to chlorthalidone group. The authors concluded
that diuretics are superior to amlodipine or lisinopril in
reducing the cardiovascular morbidity and are much less
expensive.
Comments
For decades, the search for an ideal antihypetensive has
been on. An ideal antihypertensive is one which not only
IHJ-Selected Summary.p65
98
5/6/2003, 10:08 AM
Selected Summaries 99
IHJ-Selected Summary.p65
99
5/6/2003, 10:08 AM
IHJ-Selected Summary.p65
100
5/6/2003, 10:08 AM
September 1621, 2003, Transcatheter Cardiovascular Therapeutics 2003, Washington, D.C., USA
Contact: The Course Directors
55 East 59th Street, 6th Floor
New York NY 10022-1112, USA
Tel: 1 212 434 6300
Fax: 1 212 434 6386
e-mail: info@crf.org
Cal of Conference.p65
101
Calendar of Conferences
October 2630, 2003, 69th Annual Scientific
Assembly, American College of Chest Physicians,
Orlando, Florida, USA
Contact: American College of Chest Physicians
3300 Dundee Road, Northbrook IL 60062, USA
Tel: 1 847 498 1400
Fax: 1 847 498 5460
5/6/2003, 10:08 AM