Abnormal mitral valve apparatus in a case of hypertrophic obstructive cardiomyopathy: Intraoperative transesophageal echocardiography

Hypertrophic obstructive cardiomyopathy is a relatively common disorder that signifies asymmetric hypertrophy of interventricular septum causing obstruction of the left ventricular outflow tract (LVOT). However, more recent studies have shown that during ventricular systole, flow against an abnormal mitral valve apparatus results in drag forces on the part of the leaflets. The mitral leaflet is pushed into the LVOT to obstruct it. We present a case where intraoperative transesophageal echocardiography played a crucial role in defining the etiology of LVOT obstruction that subsequently helped in deciding the surgical plan.

Pseudo-infarct in ECG in A Case of Asymmetric Septal Hypertrophy.

A 68-year-old male with a history of type 2 diabetes and hypertension presented for a routine check-up. His routine ECG revealed recent inferior infarct. He was admitted and later echocardiography showed it to as asymmetric septal hypertrophy. The ECG findings of the disease and various causes of pseudo-infarct are discussed.

A Case of Asymmetric Septal Hypertrophy Combined with Conn's Syndrome

We report a case of a 44 year old femele with unilateral aldosterone-proudcing adrenal adenoma characterized by hypertension, plasma aldosterone excess, and low plasma renin, commonly but not invariably with hypokalemia. She also had asymmetric septal hypertrophy of left ventricle established with two-dimensional echocardiography. The electrocardiogram showed inverted T wave and prominent U wave with high QRS voltage on precordial leads. In the case of this patient, we are not sure whether asymmetric septal hypertrophy was caused by secondary hypertension and chronic aldosterone excess of primary aldosteronism, or hypertrophic cardiomyopathy per se, so further long=term follow-up is required to determine it. Following the successful unilateral adrenalectomy, however, the systemic pressure fell down to the normal level and electrolyte abnormalities were corrected immediaterly within a few days and the modest regression in septal hypertrophy was noted in one year, suggesting that the promary aldosteronism contributes to the development or porgression of asymmetric septal hepertrophy.

Echocardiographic Evaluation of Regional Wall Motion Nonuniformity and Phase Difference in Asymmetric Septal Hypertrophy

BACKGROUND: A regional wall motion nonuniformity and a phase difference between LV posterior wall motion and transmitral flow are present during normal rapid filling period and are thought to be an evidence for involvement of ventricular restoring forces. To assess the role of nonuniformity on diastolic funtional impairment of asymmetric septal hypertrophy(ASH), the time relations between left ventricular regional wall motions and filling velocity were studied. METHOD: We measured the time intervals from A2 to peak rate of LV posterior wall(short axis) thinning(A2-(-)dpw/dt), peak rate of medial mitral annulus (long axis dimension) lengthening(A2-dL/dt) and peak mitral flow(A2-E) by M-mode and Doppler echocardiography. Result: In ASH patients, A2-(-)dpw/dt(106+/-6msec, mean SE) and the regional wall motion nonuniformity((-)dpw/dt-dL/dt, 89+/-11msec, mean SE) were increased significantly when compared with normal control values(88+/-4, 28+/-5msec, mean SE, p<0.01,respectively).In normal controls, peak mitral flow velocity lagged peak rate of regional wall motion, so the phase differences were present((-)dpw/dt-E :71+/-8msec, dL/dt-E:44+/-6msec). In ASH patients, (-)dpw/dt-E was present(90+/-16msec) but dL/dt-E was not present or reversed(-21+/-18 msec). So these chacteristic phase differences were disturbed. CONCLUSION: These data suggested that the relaxation nonuniformity of regional wall motion in ASH may act as an energy dissipating factor of restoring forces during rapid filling period.