We studied the physiology of pulmonary venous flow in 13 normal subjects and five patients with atrial rhythm disorders and atrioventricular conduction disturbances with pulsed Doppler and two-dimensional echocardiography. The left atrium, mitral valve, and pulmonary venous ostia were visualized through the apical four-chamber view. Mitral and pulmonary venous flows were obtained by placing the Doppler sample volume at the appropriate orifice. Pulmonary venous flow was biphasic: a rapid filling wave was observed during systole when the mitral valve was closed; a second wave was observed in diastole during the rapid ventricular filling phase of mitral flow, but was significantly delayed. In patients without atrial contraction (atrial fibrillation and sinoatrial standstill), the initial rapid filling was greatly diminished and only the second diastolic wave appeared to contribute to left atrial filling. In patients with high-grade atrioventricular block, each atrial contraction was followed by a surge in flow fromi the pulmonary veins. These results are consistent with data obtained from invasive measurements in both dogs and man, and confirm the validity of the use of pulsed Doppler echocardiography in the study of pulmonary venous flow. We suggest that pulmonary venous flow is influenced by dynamic changes in left atrial pressure created by contraction and relaxation of the atrium and ventricle. The initial peak in pulmonary venous flow occurs with atrial relaxation simultaneously with the reduction of left atrial pressure, and the second peak occurs with left ventricular relaxation and rapid transmitral filling of the ventricle. Circulation 71, No. 6, 1105-1112, 1985. THE PATTERN OF FLOW in the large extraparenchymal pulmonary veins is pulsatile in both dog and man.'-'' The pulsatile nature of pulmonary venous flow has been suggested by several investigators to result from changes in left atrial pressure occurring throughout the cardiac cycle.' 6 Others have attributed pulmonary flow to forward transmission of pressure pulses from the right ventricle through the pulmonary circulation7"'' or to a combination of the propulsive force of the right ventricle and suction created by the left heart.' I] Simultaneous invasive measurements of pulmonary vein flow and left atrial pressure in a canine preparation and in patients with aortic stenosis revealed that pulmonary vein flow velocity was maximal during the troughs and minimal during the peaks of left atrial pressure.'

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Over a 3 year period we evaluated 23 patients (16 men, seven women) with apical hypertrophic cardiomyopathy by noninvasive and invasive methods. Sixteen patients had chest pain. In 17, results of cardiovascular examination were normal. The electrocardiogram showed precordial inverted T waves in all patients and these were of mild-to-moderate amplitude (<10 mm) in 18 and giant (>10 mm) in five. M mode echocardiography revealed a typical pattem of contraction and relaxation in the apical region of the left ventricle that was associated with significant hypertrophy. These findings were confirmed by two-dimensional echocardiography. Systolic anterior motion of the mitral valve was not observed nor was there any evidence of obstruction of the left ventricular outflow tract. Results of Doppler echocardiographic study of the mitral and aortic flow were normal in all patients but one who had mild mitral insufficiency. Radionuclide studies of 14 patients revealed a mean left ventricular ejection fraction of 66 + 6% (range 55% to 79%), with normal left ventricular contraction in all patients but two with apical hypokinesis. In all six patients who underwent catheterization a characteristic appearance of the left ventricle at end-systole as well as abnormal end-diastolic contour were noted on the left ventricular angiogram, but the "ace of spades" configuration was seen in only one. We conclude that the 23 patients studied form a homogeneous group of individuals with nonobstructive apical hypertrophic cardiomyopathy, which differs in many respects from cardiomyopathies reported by other investigators. Circulation 71, No. 1, 45-56, 1985. HYPERTROPHIC CARDIOMYOPATHY is defined as a heart muscle disorder of unknown origin that is characterized by hypertrophy of a nondilated left ventricle. ' The hypertrophy may be obstructive or nonobstructive and its distribution may exhibit marked variation.2 Recently, Japanese investigators34 described a form of nonobstructive hypertrophic cardiomyopathy characterized by disproportionate hypertrophy of the left ventricular apical region associated with giant precordial negative T waves and high QRS voltage. A characteristic "ace of spades" configuration at end-diastole was observed on left ventriculograms of patients with this disorder. 5' 6 Reviewing their extensive experience with hypertrophic cardiomyopathy, Maron et pertrophy similar to that observed by the Japanese investigators. However, the electrocardiograms of their patients showed relatively mild T wave inversion and left ventricular angiograms showed a characteristic appearance of mid left ventricular constriction and a small, often poorly contracting apical segment.No other extensive study of apical hypertrophic cardiomyopathy has appeared in the literature and only a few cases have been reported with findings similar to those of the Japanese group.tt-4 The present study reports a series of 23 patients with apical hypertrophic cardiomyopathy who were evaluated at our institution by both noninvasive and invasive...