Prinzmetal's angina. Aternating ST-segment deviation in anterior and inferior electrocardiographic leads during the same episode of pain.

A 60-year-old man had recurrent episodes of spontaneously occurring pain in the chest which were associated with ST-segment elevation consistent with Prinzmetal's angina. The simultaneous elevation of the S-T segment in anterior and inferior electrocardiographic leads with initial ST-segment depression followed by elevation in high lateral leads suggested that heightened vascular reactivity in variant angina may involve multiple coronary vessels during the same episode of vasospasm.

Abnormal left ventricular contraction pattern in the systolic click-late systolic murmur syndrome.

A contraction abnormality of the left ventricle has previously been described in patients with systolic click-late systolic murmur syndrome. To determine if the contraction abnormality is present in the preprolapse period, LV dimensions and the instantaneous velocity of circumferential fiber shortening (VCF) were studied in 18 patients with the mitral valve prolapse and 16 normal subjects using computer analysis of echocardiograms. VCF attained its maximum (max VCF) during the preprolapse period an average of 94 msec before the mid-systolic click. Max VCF was significantly reduced in patients with mitral valve prolapse (2.06 vs 2.55 circ/sec in normal subjects, P less than 0.001). Despite the reduction in max VCF, no difference in the extent and percentage of diameter shortening was found between patients and normal subjects. This discrepancy is explained by a sustained rate of mid-to-late systolic diameter shortening in the presence of mitral valve prolapse as manifested by a typical VCF profile (P less than 0.001) and a longer duration of diameter shortening (353 vs 306 msec in normal subjects, P less than 0.01). The decrease of max VCF in patients with mitral valve prolapse suggests a reduction in LV contractility. Since the abnormality is present in the preprolapse period, it is unrelated to a direct mechanical effect of the prolapse itself. Additional fiber shortening in mid-to-late systole indicates that the sudden displacement of the mitral leaflets may have an unloading effect on the left ventricle.

The determinants of onset of mitral valve prolapse in the systolic click-late systolic murmur syndrome.

The onset of mitral valve prolapse and its close correlate, the time of systolic click, vary considerably with different physiologic and pharmacologic interventions. In order to explain the mechanism responsible for these alterations, the effects of tilt and amyl nitrite inhalation on left ventricular dynamics and the time of the systolic click were studied by analyzing echocardiograms and simultaneously recorded phonocardiograms in 14 patients with mitral valve prolapse and mid-systolic click. The patients were studied in the supine position, with 40-60 degrees head-up tilt and after amyl nitrite inhalation. Computer analysis of the recordings was used to measure the left ventricular end-diastolic diameter, the click diameter (left ventricular diameter at the time of mid-systolic click), the maximal velocity of circumferential fiber shortening (max VCF), and the time interval between the first heart sound and systolic click (S1-X). With tilt and amyl nitrite, shortening of the S1-X interval b y an average of 44 and 87 msec, respectively, was observed. The click diameter, however, remained virtually constant with both maneuvers. Earlier prolapse after tilt was due to a decrease in the end-diastolic diameter from 5.03 +/- 0.74 to 4.50 +/- 0.68 cm (P less than 0.001) with no change in max VCF. Immediately after amyl nitrite, earlier prolapse was due to an increase of VCF in the preprolapse period, with max VCF increasing from 2.15 +/- 0.27 to 3.06 +/- 0.40 circ/sec (P less than 0.001), there being no change in the end-diastolic diameter up to this time. The constant click diameter indicates that the abnormal valve motion in this syndrome occurs at a critical left ventricular chamber size. Variations in the onset of prolapse are caused by changes in left ventricular end-diastolic dimensions and the velocity of circumferential fiber shortening in the preprolapse period.