It seems possible, therefore, that the real but "unusual" occurrence of diaphragmatic pacing in other cases could be explained by otherwise asymptomatic pedoration of the pacemaker electrode. This becomes all the more likely when one considers that the right ventricular myocardium is 4 to 5 mm thick and the electrode tip of the pacemaker employed in our case is a platinum knob 10 mm long. Certainly, radiologic changes and alterations in the spike potential as measured on the sudace electrocardiogram would not be consistent with an only slight change in position such as most probably occurred with the partial pedoration in our case. B. Hurwitz, M.D., B.Ch. Johannesburg, South Africa
Echocardiographic Diagnosis of Idiopathic Hypertrophic Subaortic Stenosis To the Editor: Kossowsky et al (Chest, 64:529, 1973) recently reported a case of IHSS with acute myocardial infarction. A 61-year-old man was admitted to the Kaiser Sunset Hospital with crushing substernal and left chest pain. Serial ECGs and SGOTs were compatible with an acute anterior myocardial infarction. During the first three days of hospitalization no heart murmur was noted. After the third day, a grade 3-4/6 apical and left sternal border systolic murmur with transmission to the neck vessels was noted. This murmur was similar to a heart murmur noted for several years in the outpatient department. Because of the disappearance of the murmur echocardiography was pedormed and was diagnostic of IHSS. The septal to posterior left ventricular wall thickness had a ratio of 1.8, and there was early systolic closure of the aortic leaflets (Fig 1), typical systolic anterior movement, and a low normal diastolic closure rate of the anterior leaflet of the mitral valve. A rapid upstroke of the carotid pulse was present.
Mitral insufficiency murmurs often appear during acute myocardial infarction because of elevated left ventricular end diastolic pressure, papillary muscle dysfunction, or papillary muscle or chordae rupture. The disappearance of such a murmur during acute myocardial infarction led, in this case, to the suspicion of IHSS which was confirmed by echocardiography. The systolic murmur of IHSS in myocardial infarction might be expected to decrease because of the decreased myocardial contractility, increased left ventricular volume, and decreased left ventricular systolic pressure. The echocardiogram presented by Kossowsky et al appears to show a normal septal thickness of about 10 mm, and the quality of the mitral valve echo, although suggestive of, is not diagnostic of IHSS. The early systolic left ventricular outflow obstruction was demonstrated by left heart catheterization, carotid pulse trace, and apex cardiogram, but in the absence of a diagnostic echocardiogram and with the subsequent disappearance of the obstruction possibly was secondary to a disorder other than IHSS. Lewis Sasse, M.D., Department of Internal Medicine Southern California Permanente Medical Group, Los Angeles
To the Editor: We were pleased to read Dr. Sasse's letter reporting another patient with both acute myocardial infarction and idiopathic hypertrophic subaortic stenosis. His objection to our echocardiogram, as labelled, for support of the diagnosis of idiopathic hypertrophic subaortic stenosis is a valid one. However, careful review of our echocardiogram does in fact reveal an abnormally thickened septum of 1.8 em. We do apologize for the mislabeling. Waffen A. Kossowsky, M.D. and George E. Gabor, M.D., Brookdale Hospital Medical Center, Brooklyn
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FxcURE 1. Echocardiogram showing systolic anterior movement of the anterior leaflet of the mitral valve. ECG = electrocardiogram; ALMV = anterior left leaflet mitral valve; PLMV = posterior leaflet mitral valve; PLV =posterior left ventricle.
466 COMMUNICATIONS TO THE EDITOR
CHEST, 66: 4, OCTOBER, 1974