Franz Schwarz

The effect of aortic valve replacement on survival.

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 inpatients 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.

Reduced coronary dilatory capacity and ultrastructural changes of the myocardium in patients with angina pectoris but normal coronary arteriograms.

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.

Reduction of coronary reserve: a mechanism for angina pectoris in patients with arterial hypertension and normal coronary arteries.

The pathogenesis of angina pectoris in patients with left ventricular hypertrophy secondary to arterial hypertension and with normal coronary arteries remains uncertain. We measured coronary blood flow (argon method) in 12 control subjects and in 16 patients with arterial hypertension at rest and after intravenous administration of dipyridamole (0.5 mg/kg). In the patients with arterial hypertension, coronary blood flow response to dipyridamole was markedly reduced (p less than .001 as compared with control values). During coronary vasodilation there was a linear correlation between coronary resistance and left ventricular end-diastolic pressure (r = .67, p less than .001). Left ventricular catheter biopsy specimens did not reveal alterations in myocardial microvasculature. These findings suggest that reduction of coronary reserve may be an important contributor to the pathogenesis of angina pectoris in these patients.

Ventricular arrhythmias in idiopathic dilated cardiomyopathy.

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.

Determinants of survival in patients with congestive cardiomyopathy: quantitative morphologic findings and left ventricular hemodynamics.

We analyzed data from 68 consecutive patients with congestive cardiomyopathy to evaluate the prognostic significance of quantitative morphologic findings in left ventricular myocardium as compared with the prognostic significance of left ventricular hemodynamics. Left ventricular endomyocardial biopsy specimens were obtained from all patients during diagnostic heart catheterization. Myocardial fiber diameter, volume fraction of interstitial fibrosis, and intracellular volume fraction of myofibrils were determined by light-microscopic morphometry. All patients had normal coronary arteriograms, but reduced left ventricular ejection fractions. There were 23 deaths during a mean follow-up period of 1124 days. Multivariate regression analysis (Cox model) revealed that left ventricular ejection fraction (p less than .00001) and left ventricular systolic pressure (p less than .01), but not morphometric findings in biopsy specimens, were independent predictors of cardiac death. Thus, morphologic findings in the left ventricular myocardium do not contribute significantly to the prognostic evaluation in patients with congestive cardiomyopathy studied by hemodynamic and angiographic methods.

Quantitative morphologic findings of the myocardium in idiopathic dilated cardiomyopathy

This study assesses the relation between quantitative morphologic findings and left ventricular contractile function in patients with idiopathic dilated cardiomyopathy. Left ventricular endomyocardial catheter biopsy specimens were obtained from 73 patients during diagnostic heart catheterization. All patients had normal coronary arteriograms but abnormal electrocardiograms. Twenty-six patients had normal left ventricular function (ejection fraction greater than or equal to 55%), whereas 47 patients had contractile dysfunction (ejection fraction less than or equal to 54%). Myocardial fiber diameter, volume fraction of interstitial fibrosis, and intracellular volume fraction of myofibrils were determined by light microscopic morphometry. Results of light microscopic morphometry were confirmed by electron microscopic morphometry in 12 patients. The coefficient of variation (analysis of several biopsies from the same patient) was 6% for determination of fiber diameter, 43% for interstitial fibrosis, and 3% for volume fraction of myofibrils. Fiber diameter (r = -0.32, p less than 0.01) and fibrosis (r = -0.47, p less than 0.001) showed a negative correlation, the volume fraction of myofibrils (r = 0.55, p less than 0.001) and calculated myofibrillar mass per 100 g of myocardium (r = 0.64, p less than 0.001) a positive correlation with the ejection fraction. Thus, (1) sampling error is low for determination of fiber diameter and myofibrils but high for evaluation of fibrosis, and (2) a reduction in the volume fraction of myofibrils and an increase in fibrosis are morphologic correlates of left ventricular dysfunction in patients with idiopathic dilated cardiomyopathy.

Coronary dilatory capacity in idiopathic dilated cardiomyopathy: analysis of 16 patients.

Hemodynamic function and overall coronary blood flow (argon technique) were measured in 16 patients with idiopathic dilated cardiomyopathy (IDC) and in 12 patients without detectable heart disease (control subjects) referred for precordial pain. In patients with IDC, coronary blood flow was normal at rest (78 +/- 17 ml/100 g-min versus 78 +/- 9 in control subjects). During maximal inducible coronary vasodilation (dipyridamole, 0.5 mg/kg), coronary blood flow was significantly reduced (142 +/- 38 ml/100 g.min versus 301 +/- 64 in control subjects; p less than 0.001). Consequently, obtainable minimal coronary resistance was increased in IDC (0.54 +/- 0.20 mm Hg/ml/100 g.min versus 0.23 +/- 0.04 in control subjects; p less than 0.001). In patients with IDC, left ventricular (LV) end-diastolic pressure was significantly increased (19 +/- 11 mm Hg versus 6 +/- 3 in control subjects; p less than 0.005), and the LV ejection fraction was diminished (36 +/- 11% versus 72 +/- 3% in control subjects; p less than 0.001). In patients with IDC, LV end-diastolic pressure correlated significantly with the obtained minimal coronary resistance after application of dipyridamole (r = 0.85; p less than 0.001). LV catheter biopsy specimens revealed no alterations in myocardial microvasculature. Thus, coronary dilatory capacity is impaired in patients with IDC, due partially to an increase in extravascular component of coronary resistance.

Intracoronary thrombolysis in acute myocardial infarction: Correlations among serum enzyme, scintigraphic and hemodynamic findings

Abstract The effect of early reperfusion after intracoronary infusion of streptokinase in patients with acute myocardial infarction was assessed in 27 patients by serial analysis of serum creatine kinase (CK) activity, thallium-201 scintigraphy (seven pinhole technique) and left ventricular and coronary angiography. Serial serum CK activity determinations were carried out at hourly intervals. Thallium-201 tomographic scintigrams were obtained before and 24 hours after recanalization. The size of the perfusion defect was measured from eight scintigraphic cross sections of the left ventricle. Regional ejection fraction was determined from the left ventricular angiogram before and 4 weeks after recanalization. The results in three groups of patients are presented: group A, 10 patients with successful recanalization and a peak serum CK activity of less than 1,000 U/liter; group B, 9 patients with successful recanalization and a peak serum CK activity of more than 1,000 U/liter and group C, 8 patients with unsuccessful recanalization. Patients in group A showed an increase in CK activity (from 46 to 603 U/liter p p p p p p > 0.05). Patients in group C had an increase in serum CK activity (from 43 to 1,756 U/liter, p p > 0.05) and no change in regional ejection fraction (from 32 to 26 percent, p >0.05). Compared with patients in group B, those in group A had a shorter duration of ischemia (3.9 versus 4.8 hours), more frequently adequate collateral supply to the infarcting area before recanalization (40 versus 0 percent of patients) and a smaller area supplied by the occluded vessel (115 versus 141 °). Although all differences were not at the level of significance ( p > 0.05), conditions for tolerating ischemia were better in group A than in group B. The study shows that early reperfusion has a beneficial effect on the extent of myocardial necrosis as estimated from serum enzyme determinations, thallium-201 scintigraphy and contrast ventriculography. The beneficial effect depends on the duration of myocardial ischemia and on the blood supply to the ischemic area by collateral vessels.

Thrombolysis in acute myocardial infarction using intracoronary streptokinase: assessment by thallium-201 scintigraphy.

Twenty-one patients with acute myocardial infarction, admitted to the hospital within 4 hours after the onset of symptoms, were studied by seven-pinhole thallium-201 scintigraphy before and I hour and 24 hours after intracoronary fibrinolysis using streptokinase. The size of the thallium-201 perfusion defect was assessed from myocardial cross sections reconstructed from the original seven-pinhole data and expressed as a fraction of left ventricular circumference.Recanalization was achieved in 16 patients within 3.9 ± 1.6 hours after onset of symptoms (group A). In these patients, the size of the perfusion defect had decreased from 36 ± 17% to 19 ± 15% (p < 0.001) at 24 hours. No significant change was detected by redistribution at 1 hour after the intervention. In five patients, intracoronary fibrinolysis was unsuccessful, and the vessel remained occluded (group B). The thallium-201 perfusion defect affected 40 ± 15% of the left ventricular circumference before the intervention; it remained virtually unchanged at 1 hour (37 ± 16%) and at 24 hours (41 ± 15%) after fibrinolysis. The perfusion defect was most reduced in patients with extensive collaterals supplying the ischemic area or with subtotal occlusion of the affected coronary artery.We conclude that successful intracoronary fibrinolysis may reduce the size of the thallium-201 perfusion defect in many patients with acute myocardial infarction. One important factor in the final result may be the presence of residual coronary flow supplied by extensive collaterals or by subtotal occlusion of the affected coronary artery when reperfusion is achieved around 4 hours after the onset of symptoms.

Influence of reperfusion on serum concentrations of cytosolic creatine kinase and structural myosin light chains in acute myocardial infarction.

The kinetics of cytosolic and structural marker protein release from myocardium were studied in 44 patients with acute myocardial infarction. After intracoronary infusion of streptokinase, there was early recanalization of the infarct-related artery in 8 patients and late recanalization in 18. In 18 patients the infarct-related artery remained occluded. Creatine kinase (CK) level peaked and normalized significantly earlier in patients with early reperfusion than in patients with late reperfusion, and in patients with late reperfusion earlier than in patients with permanent occlusion. Thus, the interval of absolute diagnostic sensitivity of CK depends on early infarct perfusion. In contrast, release of myosin light chains was not significantly changed by recanalization of the infarct-related artery compared with that in nonreperfused myocardial infarction. Thus, in patients with acute myocardial infarction, myosin light chains may be superior to CK as a diagnostic means and for estimation of infarct size.