CASE REPORT

Systolic Flow Reversal in a Case of Mid-Ventricular

Obstructive Hypertrophic Cardiomyopathy
Ikuo Misumi 1, Tsuyoshi Honda 1, Hirofumi Kurokawa 1, Yuji Kubota 1, Masanobu Ishii 2,
Ryota Sato 2, Hiroshige Yamabe 2, Hisayo Yasuda 2, Koichi Kaikita 2,
Seiji Hokimoto 2 and Hisao Ogawa 2

Abstract
A 69-year-old man presented to our hospital with chest pain. Two-dimensional transthoracic echocardiography showed hypertrophy of the left ventricle, mid-ventricular obstruction and an apical aneurysm. Color-flow
imaging at the obstruction site on the apical four-chamber view demonstrated systolic flow reversal in addition to a paradoxical jet flow. The systolic flow reversal may have been caused by a decreased apical contractility and pressure during systole.
Key words: systolic flow reversal, mid-ventricular obstruction, Doppler echocardiography
(Intern Med 54: 1765-1769, 2015)
(DOI: 10.2169/internalmedicine.54.4153)

Introduction
Apical aneurysms may be present in patients with midventricular
obstructive
hypertrophic
cardiomyopathy
(MVOCM) (1) and are frequently associated with an unusual type of intraventricular isovolumetric relaxation flow
called a paradoxical jet flow (2). We herein report a rare
case of MVOCM associated with additional systolic flow reversal from the base of the ventricle (LV) to the apex.

Case Report
A 69-year-old man presented to our hospital after experiencing chest pain and a transient loss of consciousness
while driving a taxi. His blood pressure was 140/95 mmHg
and his pulse rate was 87 beats/min. Auscultation showed a
Levine 2/6 systolic murmur at the right upper sternal border,
while a 12-lead electrocardiogram (ECG) showed a sinus
rhythm with complete right bundle branch block and negative T waves. In addition, a chest radiograph disclosed a cardiothoracic ratio of 0.52, and two-dimensional transthoracic
echocardiography revealed hypertrophy of the left LV (inter-

ventricular septum: 14 mm thick, and LV posterior wall: 13

mm thick) as well as mid-ventricular obstruction and an apical aneurysm (Fig. 1). Continuous-wave Doppler echocardiography of the site of obstruction (Fig. 2) and color-flow
imaging in the apical four-chamber view (Fig. 3) demonstrated systolic mid-ventricular obstruction and a paradoxical
jet flow typical of MVOCM. Furthermore, there was a systolic flow reversal from the LV base to the apex between the
systolic and paradoxical jet flow (Fig. 2, 3), and cardiac
MRI imaging showed massive LV hypertrophy and midventricular obstruction (Fig. 4, right panel, arrows).
The patient underwent cardiac catheterization. Although
no significant coronary artery stenosis was observed, coronary spasms were induced by the intracoronary injection of
acetylcholine. The patients hemodynamic data showed a
mean pulmonary capillary wedge pressure of 12 mmHg, LV
end-diastolic pressure of 25 mmHg, cardiac output of 5.5 L/
min and cardiac index of 2.6 L/min/m2. There were no significant peak systolic pressure gradients in the LV apex, LV
base or aorta (Fig. 5).
The patient was subsequently treated with a calcium
channel blocker and angiotensin II receptor blocker and discharged from our hospital.

Department of Cardiology, Kumamoto Saisyunsou Hospital, Japan and Department of Cardiovascular Medicine, Kumamoto University School
of Medicine, Japan
Received for publication September 24, 2014; Accepted for publication November 19, 2014
Correspondence to Dr. Ikuo Misumi, misumi@saisyunsou1.hosp.go.jp

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DOI: 10.2169/internalmedicine.54.4153

Figure1.Apical four-chamber view in diastole (left panel) and systole (right panel) shows an apical
aneurysm (An.) and mid-ventricular obstruction (arrows).

Figure2.Continuous Doppler echocardiography at the site of left ventricular obstruction shows

mid-systolic flow reversal (a) and a paradoxical jet flow (b).

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DOI: 10.2169/internalmedicine.54.4153

Figure3.Color-flow imaging in the apical four-chamber view in systole (left panel), late-systole
(middle panel) and isovolumetric relaxation (right panel) during the cardiac cycle. Systolic flow reversal is observed between the systolic forward flow and paradoxical jet flow.

Figure4.Cardiac MRI imaging shows massive LV hypertrophy with mid-ventricular obstruction

(arrows).

Discussion
MVOCM may be accompanied by apical aneurysm formation. Although the precise pathogenesis of apical aneurysms is unknown, these lesions may be caused by high apical pressure due to mid-ventricular obstruction (3).
Another proposed mechanism underlying aneurysm formation is myocardial ischemia. The oxygen supply may decrease as a result of an impaired coronary flow reserve, de-

creased coronary perfusion pressure, squeezing of the coronary arteries and coronary spasms (4, 5). The oxygen demand is also increased by high apical pressure and wall
stress (6).
Moreover, enlargement of the apex and thinning of the
wall caused by aneurysm formation may increase wall
stress, which subsequently induces positive feedback, thus
leading to a vicious cycle (Fig. 6).
This case may be the second reported case demonstrating
additional transient mid-systolic flow reversal between the

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DOI: 10.2169/internalmedicine.54.4153

Figure5.Pressure recording during cardiac catheterization (lower panels). The upper panels show
the positions of pressure recording. There were no significant peak pressure gradients in the LV apex
(left panel), LV base or aorta.

Figure6.Pathogenesis underlying the formation of a left ventricular apical aneurysm in the setting
of mid-ventricular obstructive hypertrophic cardiomyopathy (MVOCM).

systolic flow and a paradoxical jet flow. We previously encountered a case of atrial fibrillation in a patient with
MVOCM and systolic flow reversal, suggesting that atrial
fibrillation contributes to the development of this unusual
flow (7). However, the present patient had a sinus rhythm.
We therefore consider that the systolic flow reversal may

have been caused by a decrease in the systolic apical pressure equal to the LV basal pressure as a result of hypokinesis of the apex (Fig. 6, left lower).
In conclusion, we herein reported a rare case of systolic
flow reversal in a patient with MVOCM exhibiting an apical
aneurysm.

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DOI: 10.2169/internalmedicine.54.4153

The authors state that they have no Conflict of Interest (COI).

References
1. Maron MS, Finley JJ, Bos JM, et al. Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in
hypertrophic cardiomyopathy. Circulation 118: 1541-1549, 2008.
2. Hanaoka Y, Misumi I, Rokutanda T, et al. Simultaneous pressure
recording in mid-ventricular obstructive hypertrophic cardiomyopathy. Intern Med 51: 387-390, 2012.
3. Matsubara K, Nakamura T, Kuribayashi T, et al. Sustained cavity
obliteration and apical aneurysm formation in apical hypertrophic
cardiomyopathy. J Am Coll Cardiol 42: 288-295, 2003.

4. Sato Y, Matsumoto N, Matsuo S, Yoda S, Kunimoto S, Saito S.

Mid-ventricular hypertrophic obstructive cardiomyopathy presenting with acute myocardial infarction. Tex Heart Inst J 34: 475478, 2007.
5. Harada K, Shimizu T, Sugishita Y, et al. Hypertrophic cardiomyopathy with midventricular obstruction and apical aneurysm: a
case report. Jpn Circ J 65: 915-919, 2001.
6. Grossman W, Jones D, McLaurin LP. Wall stress and patterns of
hypertrophy in the human left ventricle. J Clin Invest 56: 56-64,
1975.
7. Ito M, Misumi I, Rokutanda T, et al. Mid-systolic flow reversal in
a patient with mid-ventricular obstructive hypertrophic cardiomyopathy. J Echocardiogr 12: 78-80, 2014.

2015 The Japanese Society of Internal Medicine

http://www.naika.or.jp/imonline/index.html

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