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that has gotten progressively worse over the last several weeks. He says that approximately a year ago the pain would occasionally occur when he was mowing his yard but now the pain sometimes occurs while he is sitting in a chair at night reading a book. The pain which is localized over the sternum lasts much longer now than it did a few months ago.
present?
Myocardial Ischaemia
An imbalance between the supply of oxygen and the
hemoglobin and systemic oxygenation When atherosclerotic disease is present, the artery lumen is narrowed and vasodilatation is impaired Coronary blood flow cannot increase in the face of increased demands and ischemia may result
anaerobic metabolism, with a progressive impairment of metabolic, mechanical, and electrical functions. Angina pectoris is the most common clinical manifestation of myocardial ischemia. It is caused by chemical and mechanical stimulation of sensory afferent nerve endings in the coronary vessels and myocardium. During ischemia, ATP is degraded to adenosine, which, thay diffuses to the extracellular space, causing arteriolar dilation and anginal pain. Adenosine as a pain messenger: Adenosine induces angina mainly by stimulating the A1 receptors in cardiac afferent nerve endings.
The coronary blood flow may be reduced by a mechanical obstruction due to - atheroma - thrombosis - spasm - embolus - coronary ostial stenosis - coronary arteritis
There can be reduction in the flow of oxygenated blood due to :- Anaemia - Carboxyhaemoglobinaemia - Hypotension Increased demand for oxygen occurs in:- increase cardiac output (e.g. thyrotoxicosis) - myocardial hypertrophy (e.g.hypertension or aortic stenosis)
Angina
When ischemia results it is frequently accompanied by
chest discomfort associated with abnormal myocardial function in the absence of myocardial necrosis
duration of ischemic episodes occurring at lower workloads than previously or even at rest In the majority of patients with angina, development of myocardial ischemia results from a combination of fixed and vasospastic stenosis
Risk factors
Risk factors
a. ECG b. serum cardiac enzymes c. Lipid profile d. chest x-ray e. coronary angiogram
Laboratory Investigations
- Specimen Collection:
Serum is the specimen of choice Heparinized plasma is acceptable
- Collection Time:
Serial specimens collected at appropriate time
intervals
Serial measurements are most useful
Samples are drawn on admission
at 2-4 hours
at 6-8 hours
at 12 hours
or
without Low HDL-C Low Total Cholesterol with Low or Normal HDL Isolated Low HDL Isolated High LDL Lp (a) Lipoprotein Excess
200-500 mg/dl
Evaluate for risk factors:
Alcoholism Diabetes Mellitus Glycogen Storage Disease Hypertension Hyperuricemia Hypothyroidism Medications Oral contraceptives Pancreatitis Pregnancy Renal disorder
Diet
No riskfactors
Diet Retest in 1 yr
RISK FACTORS Cerebrovascular disease Cigarettes >10/day Diabetes mellitus FH of CHD/vascular disease Hypertension Male Occlusive peripheral vascular disease Overweight >30%
MYOGLOBIN
low-molecular-weight heam-containing protein
found in both skeletal and cardiac muscle. Typical rise occurs within 2-4 hours after the onset of acute myocardial infarction. This is useful for the early diagnosis of acute myocardial infarction, as this rise is generally earlier than used cardiac markers. myoglobin is not cardiac specific, better used in conjunction with other markers.
phosphate production and utilization within contractile tissues. Cytoplasmic CK is a dimer, composed of M and/or B subunits, which associate forming CK-MM, CK-MB and CK-BB isoenzymes Cytosolic CK regenerate ATP from ADP, using PCr. There are two mitochondrial creatine kinase isoenzymes, Mitochondrial creatine kinase is directly involved in formation of phospho-creatine (PCr) from mitochondrial ATP,
CK
CK-MM is the main isoenzyme found in striated
muscle CK-MB is found mainly in cardiac muscle Trace amounts of CK-MB are found in skeletal muscle. CK-BB is the predominant isoenzyme found in brain, colon, ileum, stomach and urinary bladder.
CK
Most of the CK released after a myocardial infarction
is, in fact, the MM isoenzyme CK-MM. A raised plasma total CK activity, due to entirely CKMM, may follow recent intramuscular injection, exercise or surgery (NON SPECIFIC) limited prognostic value
CK
CK-MB also exists as two isoforms, namely CK-MB1
and CK-MB2. CK-MB2 is predominantly released from the myocardium. CK-MB that is routinely assayed reflects the sum of the two isoforms. Normally CK-MB1 predominates in plasma, but after an acute myocardial infarction this is reversed. CK- MM has longer half life than MB.
CK
Plasma enzyme activity is raised in about 95 % of
cases of myocardial infarction and are sometimes very high. second rise of plasma enzyme extension of the damage A prolonged rise in plasma CK may suggest a cardiac ventricular aneurysm . plasma enzyme activity does not usually rise significantly after episode of angina pectoris without infarction.
be seen until 4-8 h after the onset of chest pain. When the diagnosis is not obvious, an elevated CK-MB or an increase in CK-MB of more than 15% over a 4-h period, even if both values are within the reference range, are suggestive of myocardial infarction. The detection of a trend by serial measurements, may provide more information than single measurements.
AST
Hepatic congestion due to right-sided heart dys-
function may contribute to the rise of plasma AST activity If there is primary hepatic dysfunction, plasma AST rises whereas LDH1 activity usually remains normal. The sequence of changes in plasma AST activity in MI are similar to those of CK .
value in the management of patients with suspected myocardial infarction. Exceptionally, when a patient with chest pain presents late, measurement of LDH may be helpful as this enzyme remains elevated in the plasma for several days following myocardial infarction.
CARDIAC TROPONIN
Cardiac troponins have been recommended as the
biochemical cardiac marker of choice. Troponins are muscle-regulator/ proteins present in skeletal and cardiac muscle. Three troponins (TnC), (Tnl) and (TnT). Tn I and TnT appear in the plasma 48 hours after symptoms of acuteMI, and are best measured 12 hours after the start of chest pain useful in the late presentation of chest pain. An increased Tnl or TnT concentration is a sensitive marker of occult myocardial damage.
CARDIAC TROPONIN
An increased Tnl or TnT concentration is a sensitive
marker of occult myocardial damage even in nonischaemic conditions. Troponin T may be elevated in patients with chronic renal failure and thus may not be so cardiac-specific
CARDIAC TROPONIN
They are therefore not early markers of acute
myocardial infarction, but they do stay elevated for about 7-10 days in plasma, which makes them useful in the late presentation of chest pain
The 3 components of Troponin complex : Troponin C = Ca++ binding. 2. Troponin I = Actinomyosin ATPase inhibiting element. * It binds actin inhibiting its binding to myosin * It is encoded by 3 different genes, giving rise to 3 isoforms. - Slow Skeletal Muscle - Fast
1.
- Cardiac
Cardiac Muscle
* It is released within 4 hrs of the onset of ischemic Symptoms of myocardial infarction. So, it is used as a marker of myocardial infarction. peaks 14-24hrs and remains elevated for 3-5 days.
3. Troponin T = Tropomyosin binding element Its level increases within 6 hours of myocardial infarction. Peaks at 72 hrs remains elevated 7-10 days. 2 Isoforms in the heart TnT1+ TnT2 are used as cardiac markers.
actin
troponin
Ca2+
Ca2+
Ca2+ Ca2+
the calcium ions bind to the troponin and changes its shape
Ca2+
Ca2+
Ca2+ Ca2+
the troponin displaces the tropomyosin and exposes the myosin binding sites
Ca2+
Ca2+
Ca2+ Ca2+
the bulbous heads of the myosin attach to the binding sites on the actin filaments
Ca2+
Ca2+ Ca2+
the myosin heads change position to achieve a lower energy state and slide the actin filaments past the stationary myosin
Pi Pi Pi A
Pi Pi Pi Ca2+ A
Ca2+
Pi Pi Pi A
Ca2+
Pi Pi Pi A Pi Pi Pi A Pi Pi Pi A
Ca2+
Ca2+ Ca2+
Pi Pi Pi A Pi Pi Pi A Pi Pi Pi A
Ca2+
Ca2+
Ca2+
Pi Pi Pi A Pi Pi Pi A Pi Pi Pi A
the troponin reverts to its normal shape and the tropomyosin move back to block the myosin binding sites
Ischaemia-modified albumin
A new marker, ischaemia-modified albumin, is raised
in the presence of myocardial ischaemia and may be used in the future in conjunction with conventional cardiac markers.
Increased coronary artery disease risk is least correlated with the following EXCEPT: a. elevated total cholesterol levels b. elevated LDL levels c. elevated HDL levels d. elevated Lipoprotein (a) levels e. elevated triglyceride levels
Increased coronary artery disease risk is least correlated with the following EXCEPT: a. elevated total cholesterol levels b. elevated LDL levels c. elevated HDL levels d. elevated Lipoprotein (a) levels e. elevated triglyceride levels
within the next 3 to 8 hours : a. Creatine kinase (CK) b. Lactic dehydrogenase (LDH) c. LDH - 1 d. LDH 2
Which cardiac enzyme would you expect to rise within the next 3 to 8 hours : a. Creatine kinase (CK) b. Lactic dehydrogenase (LDH) c. LDH - 1 d. LDH 2
The laboratory tests that would confirm a diagnosis of myocardial infarction include:
a. LDH, CK-MB and AST b. Serum calcium, and APPT c. Sedimentation rate, and ALT d. Paul-Bunnell and serum potassium
The laboratory tests that would confirm a diagnosis of myocardial infarction include:
a. LDH, CK-MB and AST b. Serum calcium, and APPT c. Sedimentation rate, and ALT d. Paul-Bunnell and serum potassium
Elevation of which of the following serum enzyme markers would be most useful in diagnosing a myocardial infarction in a patient who comes to your office 3 days after an episode of severe and prolonged substernal chest pain?
a. LDH isoenzymes b. CK.MB c. TroponinI d. myoglobin
Elevation of which of the following serum enzyme markers would be most useful in diagnosing a myocardial infarction in a patient who comes to your office 3 days after an episode of severe and prolonged substernal chest pain?
a. LDH isoenzymes b. CK.MB c. TroponinI d. myoglobin
the saturated fat in the diet and substitutes made of polyunsaturted fat is desired. When teaching the client about this diet the one should instruct the patient to avoid :
a. b. c. d.
the saturated fat in the diet and substitutes made of polyunsaturted fat is desired. When teaching the client about this diet the one should instruct the patient to avoid :
a. b. c. d.
myocardial infarction
Many patients with myocardial infarction have a
typical history of crushing central chest pain, perhaps radiating to the arm or jaw, associated with typical ECG changes. myocardial infarction can, however, present atypically, or even be clinically silent, particularly in the elderly
plasma 4-8 hours after symptoms of acute myocardial infarction, and are best measured 12 hours after the start of chest pain. They are therefore not early markers of acute myocardial infarction, but they do stay elevated for about 7-10 days in plasma, which makes them useful in the late presentation of chest pain