SUMMARY We retrospectively studied 252 operated and 47 unoperated patients with isolated aortic valve disease. Aortic valve replacement (AVR) was recommended to all patients based on clinical and hemodynamic data. Preoperative hemodynamic and angiographic data were similar in operated and unoperated cohorts. Seventy-one percent of patients received a Bjork-Shiley prosthesis. Operative mortality was 7% for the entire surgical series. For patients with predominant aortic stenosis (AS), survival at 3 years was 87% in operated and 21% in unoperated patients (p < 0.001). For patients with predominant aortic insufficiency (Al), the 5-year survival rate was 86% in operated and 87% in unoperated patients (NS). AVR improved long-term survival in patients with AS who had normal or impaired left ventricular (LV) function. In patients with Al and normal LV function, survival was not improved after AVR, but those with LV dysfunction who were operated on tended to survive longer (NS). Long-term survival of unoperated patients with AI was better than that in unoperated patients with AS.We conclude that AVR improves long-term survival in patients with AS who have normal or abnormal LV function, and that AVR does not change long-term survival in patients with Al, although those with LV dysfunction tended to survive longer. valve, symptoms (angina pectoris, syncope, congestive heart failure), the presence or progression of cardiac enlargement on serial chest radiographs, and abnormally low ejection fraction (EF) (54% or less as defined previously2). Categorizing patients according to predominant lesion showed that 144 patients had predominant AS (peak-to-peak transvalvular pressure gradient of 45-150 mm Hg with or without associated aortic regurgitation) and 155 patients had predominant Al (massive regurgitation documented by aortic root angiography,3 with or without peak-to-peak transvalvular pressure gradient of less than 30 mm Hg). Cardiac CatheterizationAll patients underwent right-and left-heart catheterization within 6 months before operation. A #8.5F Brockenbrough catheter was positioned by transseptal puncture into the left ventricle and a pigtail catheter (#7F) was advanced retrogradely into the aortic root. Pressures were recorded on an Oscillomink directwriting system with Statham transducers before injection of contrast material. LV end-diastolic pressure was measured after the "a" wave. The cardiac index was determined by the Fick method. Valve areas were not calculated, because cases with associated angiographically visible mild-to-moderate aortic regurgitation were placed in this AS group. Single-plane 35-mm cineangiograms of the left ventricle were filmed (50 ml Urografin 76) at 50 frames/sec, in the 300 right anterior oblique projection with a Phillips image-intensifier system. Aortic root angiography was performed to estimate the degree of aortic regurgitation.
SUMMARY Hemodynamic and metabolic studies were performed in 15 patients without heart disease (controls, group A), in 21 patients with typical stress-induced anginal pain but normal coronary and left ventricular angiograms (angina pectoris with normal arteriogram, group B), and in 10 patients with angiographically proved coronary artery disease (CAD, group C). Coronary dilatory capacity, determined by measuring total myocardial blood flow at rest and during maximal coronary vasodilatation (dipyridamole, 0.5 mg/kg i.v.), was markedly reduced in group B and C patients. In group B patients, left ventricular catheter biopsy specimens revealed no evidence of small-vessel disease, but did show histologic alterations of mitochondria. During atrial pacing, the control subjects showed no changes in myocardial lactate uptake, whereas in group B patients, myocardial lactate production occurred. In contrast to controls, patients in group B showed a significant decline in ejection fraction and circumferential fiber shortening during isometric exercise. These findings suggest that myocardial ischemia is the cause of angina pectoris in patients who have angina but normal coronary arteriograms.THE PARADOX of patients suffering from typical stress-induced anginal pain who have normal coronary and left ventricular angiograms has been reported in recent studies.1'~3 The nature of this disease is unknown, and it has been also called syndrome X.5 Myocardial ischemia that is caused by an abnormal affinity of hemoglobin for oxygen, coronary arterial spasm or occlusive disease of small coronary arteries not visualized by coronary arteriography have been suggested as possible causes of this syndrome.4' 6, 14 To evaluate further patients who have angina pectoris but normal coronary arteriograms, the following studies were performed in addition to left ventricular and coronary angiography: (1) Coronary blood flow (CBF) was measured at rest and during dipyridamoleinduced coronary vasodilatation; (2) biopsy specimens were taken from left ventricular myocardium for microscopic evaluation of intramyocardial vessels and of myocardial cells; (3) myocardial lactate metabolism was studied at rest and during atrial pacing; and (4) left ventricular function was assessed during rest and during exercise.
SUMMARY The linearity and sensitivity of the end-systolic pressure-volume (P-Ve,) relation to the inotropic state of the left ventricle were investigated in 11 patients with coronary heart disease and one patient with congestive cardiomyopathy. To minimize autonomic reflex responses, propranolol, 0.15 mg/kg, and atropine, 1 mg, were administered i.v. at the beginning of the study. Three ventriculograms were performed: at rest, after oral isosorbide dinitrate, 10 mg (systolic pressure decrease 15 mm Hg), and during infusion of methoxamine, 2 mg/min (systolic pressure increase > 10 mm Hg).The three points of the P-Ve, relation showed linearity (r 0.96). The relation between the slope k of the PVe, relation and the left ventricular ejection fraction at rest was best described by an exponential function (r = 0.94). The use of peak systolic pressure instead of end-systolic pressure showed equally good results. The intercept of the P-V,, line on the abscissa, which represents the theoretical end-systolic volume at zero pressure, was not related to the ejection fraction under control conditions. The P-Ve, relation in postextrasystolic beats was displaced toward the left (smaller end-systolic volumes) and became steeper.MYOCARDIAL fiber shortening is determined by preload, afterload and contractility, and end-systolic fiber length is inversely proportional to afterload.' In the isolated left ventricle, end-systolic fiber length is linearly related to end-systolic tension.2 In the experimental animal, the isolated left ventricle also shows a linear end-systolic pressure-volume (P-Ves) relationship that is not dependent on preload. The slope of the P-Ve, relation is determined by the contractile state and is increased by positive inotropic interventions.3Although the concept of the P-Ve, relationship has been applied for some time in animal experiments,1-4only recently has the P-Ve, relation been investigated as a means of assessing left ventricular function in man.Our study was undertaken to determine (1) whether the P-VVe, relation in man is linear; (2) the correlation between the slope k of the P-V,e relation and other variables of left ventricular function; (3) whether the theoretical volume at zero pressure (VO), i.e., the intercept of the P-Ves relation on the abscissa, reliably separates impaired from normal left ventricular func-
Twenty four hour ambulatory electrocardiograms were recorded in 60 patients with idiopathic dilated cardiomyopathy. The diagnosis was based on clinical, laboratory, and cardiac catheterisation findings. All patients had a left ventricular ejection fraction less than 0.55; in 39 it was less than 0.40. Ventricular extrasystoles were evident in all patients: they were rare in 11 (18%), moderately frequent in 24 (40%), and frequent in 25 (42%). Multiform extrasystoles were recorded in 57 patients (95%), paired ventricular extrasystoles in 47 (78%), and non-sustained ventricular tachycardias consisting of three to 19 beats in 25 (42%) of the 60 patients studied. Eight patients had more than five episodes of ventricular tachycardia a day. Patients with atrial fibrillation had the same frequency and grade of ventricular arrhythmias as those with sinus rhythm. Patients with infrequent and frequent ventricular extrasystoles could not be differentiated on the basis of the clinical or haemodynamic findings. The mean values of NYHA functional class, cardiac index, left ventricular end diastolic pressure, and ejection fraction were, however, significantly different in patients with and without ventricular tachycardia. During follow up of 12 +/- 5 months seven patients died; all seven had an ejection fraction less than 0.40. In four patients who died of congestive heart failure, but in only one of the three patients who died a sudden cardiac death, ventricular tachycardia was recorded during ambulatory monitoring. High grade ventricular arrhythmias are often seen in patients with idiopathic dilated cardiomyopathy; patients with ventricular tachycardia have more impairment of left ventricular function than patients without ventricular tachycardia; and ambulatory monitoring may be of little help in identifying patients at increased risk of sudden cardiac death.
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