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This study describes the characteristics of a prominent Doppler flow velocity signal representing intraventricular flow during left ventricular isovolumic relaxation. The flow during the isovolumic relaxation period was demonstrated in 60 subjects, including 7 with a normal heart, 26 with hypertrophic cardiomyopathy, 10 with aortic valve disease, 9 with a transplanted heart and 8 others. All had normal to hyperdynamic left ventricular systolic function with some degree of cavity obliteration as seen in the apical two-dimensional echocardiographic views. In contrast, this isovolumic relaxation period flow could not be demonstrated in the absence of cavity obliteration in any of 20 patients with either normal or diminished left ventricular systolic function. Isovolumic relaxation period flow was best recorded from the apical transducer position and was directed toward the apex in all patients. By pulsed wave, and with two-dimensional Doppler ultrasound, the isovolumic relaxation period flow originated within a narrow area in the medial portion of the left ventricle along the middle or basal segments of the interventricular septum, but was recorded over a larger area toward the apex. The peak isovolumic relaxation period flow velocity was recorded just basal to the area of cavity obliteration, usually at the level of the papillary muscles, and ranged from 0.4 to 2.3 m/s (mean of 1.0 m/s). This isovolumic relaxation period flow started with aortic valve closure and, in 50 of the 60 patients, it lasted throughout isovolumic relaxation until mitral valve opening. In the other 10 patients (all with hypertrophic cardiomyopathy), it lasted for only a part (mean 63%) of this period.(ABSTRACT TRUNCATED AT 250 WORDS)

Quantitative angiographic findings were reviewed in 40 patients with significant mitral regurgitation classified into three etiologic groups: group I, primary mitral regurgitation (prolapse, ruptured chordae); group II, mixed stenosis and regurgitation of rheumatic origin; and group III, cardiomyopathic mitral regurgitation. For patients in both groups I and II, left ventricular end-diastolic volume was directly related to regurgitant fraction, and ejection fraction was generally well maintained. In contrast, patients in group III had a depressed ejection fraction (less than 0.40) and end-diastolic volume that was disproportionately increased in relation to the degree of regurgitation. Left ventricular end-diastolic pressure was a poor indicator of severity of regurgitation in all patient groups. There was a significant negative correlation between forward cardiac index and regurgitant fraction. There was significant relation, although with considerable variation, between the normalized V wave and regurgitant fraction. The graphs of chamber size, ejection fraction and hemodynamic measures plotted against the severity of regurgitation in different patient groups provide a perspective for interpreting the findings in individual patients.

Eleven consecutive patients with recurrent ventricular arrhythmias were treated by an aggressive protocol and followed up prospectively. Arrhythmias, symptoms, and cardiac lesions were defined. Antiarrhythmic drugs were given on schedule, with blood levels determining dose; success or failure was defined by elimination or recurrence of symptomatic arrhythmias. When drug therapy failed, left ventricular aneurysmectomy was done when appropriate. Recurrent ventricular tachycardia was most frequently responsible for symptoms; coronary artery disease was the most frequent underlying disease. Symptomatic arrhythmias were eliminated in 8 of 11 patients (5 with drugs and 3 with aneurysmectomies), with a 16.5-month symptom-free average follow-up. An average of 2.9 therapeutic trials per patient was needed to control symptomatic arrhythmias. The average time from entry into the study until the start of ultimately effective therapy was 18 days. Therapy that eliminated symptoms did not eliminate all premature ventricular contractions, and occasionally even brief asymptomatic episodes of ventricular tachycardia persisted. Recurrent symptomatic ventricular arrhythmias can be controlled in many patients by rigorous application of current therapies.

99m-technetium (Tc) pyrophosphate myocardial scintigrams of 55 patients with stable angina pectoris were compared with those of 13 normal subjects. The mean scintigraphic score, obtained by averaging the blinded interpretations of four readers scoring on an integral scale from 0 to 4, was significantly higher for the patients with angina than for the control subjects (1.36 compared with 0.48, P less than 0.001). Among the patients with angina, those who had a prior myocardial infarction had a higher mean scintigraphic grade than those without a previous infarction (1.73 versus 1.15, P less than 0.005), and the mean grade in both groups was higher than that of control subjects (P less than 0.001). Radionuclide uptake was predominantly diffuse in the patients with angina pectoris (70%), although in those with greater uptake accumulation tended to be localized. Three of the 68 subjects had high levels of radionuclide uptake but no clinical evidence of acute myocardial injury. This study demonstrates that excess myocardial accumulation of 99m-Tc pyrophosphate can occur in patients with stable angina pectoris.

Between July 1974 and May 1979, 19,153 non-randomized patients without prior cardiac surgery and with chest pain were studied angiographically and enrolled in the Coronary Artery Surgery Study (CASS). The primary question addressed by this paper is: for fixed levels of coronary artery disease, are the presence and severity of angina pectoris greater for older than for younger patients? For those with the same extent of disease, older patients were more likely to have angina and to exhibit more severe symptoms. After adjustment for covariates using logistic regression analysis, age was found to be an important, independent predictor of the presence and severity of angina. There are many possible explanations for these findings, although physiologic factors related to aging, the disease process, and deconditioning associated with an increased sedentary life style seem most reasonable. Another possibility has to do with referral patterns for study and the prevalence of angina in the different age groups.

An unusual case of diverticulum of the left ventricle is presented. The most distinctive feature was the presence of a circumferential mid-ventricular contraction ring with histologic abnormalities similar to those described in patients with asymmetric septal hypertrophy. This abnormal ring of tissue obstructed emptying of the ventricular apex and isolated it from the rest of the ventricle. The obstructed apex assumed the appearance of a muscular diverticulum, and the residual portion of the ventricle was markedly diminished in volume. In addition, the abnormal mid-ventricular hypertrophy interfered with papillary muscle function, producing mitral valve prolapse and mitral regurgitation. The patient's age was equally unusual; she was 65 at the time of diagnosis, probably the oldest known patient with ventricular diverticulum. She was treated surgically by transapical myotomy and myectomy of the mid-ventricular contraction ring, in order to increase effective ventricular volume. The relationship of this entity to other types of ventricular deiverticula and aneurysms, and to hypertrophic cardiomyopathy, is discussed.

Left ventricular systolic torsion and diastolic recoil were quantified in 12 human cardiac transplant recipients with surgically implanted intramyocardial markers with the use of computer-aided analysis of biplane cineradiographic images. Measurements were performed between 6 and 16 weeks after surgery and related to the presence or absence of rejection as determined by cardiac biopsy. Torsional deformation, defined as twisting about the left ventricular long axis of the apical region with respect to the base, was characterized in terms of the rate and amplitude of systolic torsion and the rate of diastolic recoil by means of an internal reference system. Comparison of measurements before, during, and after recovery from 14 rejection episodes allowed assessment of the effects of acute reversible cardiomyopathy on left ventricular torsion and recoil. Compared with prerejection values, the amplitude of torsional deformation in the maximally deforming segment (theta max) decreased by 25% from 21.1 +/- 15.2 to 16.0 +/- 5.7 degrees (p less than .005) during acute rejection with myocyte necrosis; this was associated with significant (p less than .05) decreases in the peak systolic torsion rate (+d theta/dtmax), whereas the peak diastolic recoil rate (-d theta/dtmax) was unchanged. This suggests that the stiffness of elastic components of the myocardium may have increased, maintaining the rate of diastolic recoil when these elements are stretched less. With successful treatment of rejection episodes, the torsional deformation characteristics normalized. Heart rate, mean arterial pressure, left ventricular end-diastolic volume, stroke volume, ejection fraction, and peak left ventricular filling rate were unchanged with rejection episodes, whereas left ventricular end-systolic volume increased (p less than .05) during acute rejection and returned to normal with resolution of the rejection process. These data suggest that left ventricular torsional deformation amplitude and rate are sensitive to episodes of subclinical left ventricular dysfunction and that such intramyocardial marker techniques may provide new insights regarding the elastic properties of the ventricular myocardium and their impact on left ventricular mechanics.

Nitroprusside was used to reduce afterload in 13 patients with isolated, severe aortic regurgitation. The drug significantly lowered mean aortic pressure, pulse pressure, left ventricular end-diastolic pressure and left ventricular volume. Total ventricular, or angiographic, cardiac index was generally unaffected, but forward cardiac index was improved significantly in 8 of 13 patients. Augmentation of forward cardiac index was seen in patients with subnormal resting forward cardiac index, in patients with decidedly elevated end-diastolic pressure, and in those with depressed resting ejection fractions. Regurgitant fraction fell with nitroprusside in six patients and remained unchanged in seven. Total stroke work index was diminished in all patients. These data show that afterload reduction in patients with severe aortic regurgitation may improve hemodynamics by reducing aortic regurgitation or by improving ventricular pump function. The lowered total stroke work, reduced ventricular size and improved forward cardiac index imply that afterload reduction may benefit left ventricular failure and delay progressive ventricular dysfunction in patients with aortic regurgitation.

To study the effects of digoxin on regional left ventricular performance, continuous ventricular dynamics were assessed in nine patients with stable coronary disease. Computer-assisted analysis of the fluoroscopic motion of surgically implanted mid wall myocardial markers was used. The markers define six minor ventricular radii and outline the left ventricle. One and one-half hours after administration of 1 mg of intravenous digoxin, mean velocity of circumferential fiber shortening for all segments increased 19 percent, from 0.67 +/- 0.06 to 0.78 +/- 0.06 circumference/sec (P less than 0.01) and ejection fraction increased 4.5 percent, from 0.50 +/- 0.03 to 0.53 +/- 0.03 (P less than 0.05). Segmental velocity of circumferential fiber shortening, total segmental shortening and early segmental systolic shrtening increased in 83 percent to 91 percent of normal segments, depending on which index was used. Only 45 to 55 percent of initially abnormal segments benefited from digoxin. In general, segmental dyssynergy increased even when net ventricular function was enhanced. These results suggest that in pateints with chronic left ventricular contraction abnormalities due to coronary disease, deterioration of performance in abnormal regions after administration of digoxin may result from increased stress imposed by increased afterload and by improved segmental dynamics in more normal areas.