M. Schlepper

Myocardial structure and function in patients with aortic valve disease and their relation to postoperative results

Abstract Left ventricular angiographic studies were performed before and 6 months after aortic valve replacement with a Bjork-Shiley prosthesis in 21 patients, 5 with aortic stenosis, 8 with mixed aortic valve lesions and 8 with aortic insufficiency. The degree of myocardial fibrosis and myocardial ultrastructural changes were evaluated from transmural needle biopsy specimens obtained from the left ventricular anterior free wall at operation. Twelve patients without heart disease served as control subjects for angiographic data. Patients with aortic valve disease had a significantly higher left ventricular mass before operation than control subjects and a lower ejection fraction and mean normalized systolic ejection rate. After operation left ventricular mass decreased considerably but did not reach normal level. Ejection fraction and mean normalized systolic ejection rate became normal in all patients with aortic valve disease. The percent fibrosis determined with morphometry was significantly higher in the subendocardium than in the subepicardium of pressure-overloaded hearts (predominant stenosis) (19 versus 13 percent) but equal in both layers of volume-overloaded hearts (predominant regurgitation) (19 versus 18 percent). Electron microscopy revealed significant intracell alterations of the nucleus, sarcomeres, mitochondria and cytoplasmic reticulum. When all patients, regardless of type of aortic valve lesion, were considered, there was no significant correlation before operation between percent fibrosis and ejection fraction ( r 0.10) or mean normalized systolic ejection rate ( r 0.02) but a significant inverse relation between left ventricular mass and ejection fraction ( r 0.54) as well as mean normalized systolic ejection rate ( r 0.49). These data suggest that (1) Depressed left ventricular function in aortic valve disease is associated with ultrastructural degenerative cell changes, but complete recovery of cardiac function after aortic valve replacement is not prevented by these changes. (2) Interstitial myocardial fibrosis is not a primary determinant of depressed cardiac function in aortic valve disease.

Impaired left ventricular function in chronic aortic valve disease: survival and function after replacement by Björk-Shiley prosthesis.

Postoperative survival and left ventricular function were studied in 128 patients who underwent isolated aortic valve replacement by the Bj6rk-Shiley valve between 1973 and 1977. The average follow-up was 2.1 years. Patients with associated coronary artery disease or mitral valve disease were excluded. Preoperative ejection fraction ranged from 15-84%. Forty-two patients were restudied by cardiac catheterization 9.1 ± 1.1 months (mean ± SEM) after valve replacement. The hospital mortality was 11%. Preoperative type of valve lesion, functional class, cardiothoracic ratio, and ejection fraction (EF) had no significant effect on postoperative survival up to 4 years. After operation, left ventricular mass (LVMI) and peak systolic wall stress (PSWS) fell significantly, while EF and mean normalized systolic ejection rate (MNSER) increased in aortic stenosis and in aortic insufficiency. Neither in aortic stenosis nor in aortic insufficiency was there a significant relation between preoperative ejection fraction and postoperative LVMI, EF, MNSER and PSWS. We attributed this to a marked improvement of left ventricular function in patients with preoperative impaired ventricular function. Six patients with paravalvular leak at restudy had a significantly lower EF and MNSER, and a higher PSWS than patients without leak. Patients without leak had normal EF, MNSER and PSWS when compared with 10 normal persons, but LVMI remained moderately elevated. Postoperative transprosthetic gradient was 11.9 mm Hg (range 0-64 mm Hg).We conclude that impaired cardiac function is completely restored after aortic valve replacement by Bjork- Shiley valve, if valve function is good. Patients with impaired cardiac function preoperatively did not have a poorer prognosis after operation than patients with normal function.

Failure of aneurysmectomy to improve left ventricular function.

Biplane left ventricular angiography was performed in 22 patients with isolated obstructive disease of the anterior descending branch of the left coronary artery and with an anterior aneurysm following transmural myocardial infarction. Six patients were restudied between 6 and 10 months after aneurysmectomy. Left ventricular reserve was estimated by analysis of a spontaneous postextrasystolic beat. Using angiographic techniques a contractile section, a transitional section, and a noncontractile section were identified. From the surgical patients the excised aneurysm and a transmural needle biopsy of the transitional section were investigated by light microscopy. With increasing volumes of noncontractile and transitional sections, total end-diastolic volume (r = 0.81, P less than 0.001) and end-systolic volume (r = 0.94, P less than 0.001) increased linearly, while the ejection fraction decreased (r = 0.70, P less than 0.001). No relation was found between the combined volumes of the noncontractile and transitional sections on the one hand, and the end-diastolic volume, the end-systolic volume, or the ejection fraction of the contractile section on the other hand. After aneurysmectomy a significant decrease was found in end-diastolic volume (194 to 133 ml/m2, P less than 0.001) and end-systolic volume (124 to 83 ml/m2, P less than 0.001) but no change occurred in ejection fraction (35 to 37%) and left ventricular end-diastolic pressure (23 to 25 mmHg). Surgical resection included part of the transitional section, which before surgery had an average ejection fraction of 27 per cent during a normal beat, rising to 41 per cent in a postextrasystolic beat. The transitional section after surgery now formed a large akinetic area of the anterior wall. We conclude that aneurysmectomy in isolated left anterior descending artery disease with anterior aneurysm fails to improve left ventricular function because the effect of reduction of left ventricular volumes is offset by the destruction of contractile behaviour in the transitional section.

Effect of coronary stenosis on myocardial function, ultrastructure and aortocoronary bypass graft hemodynamics.

Abstract The relation between different degrees of stenosis of the left anterior descending coronary artery and total and regional left ventricular function, myocardial ultrastructure, flbrotic content of the myocardium and hemodynamics of graft flow was studied in 70 patients with coronary artery disease. Patients with arteriographically visible collateral supply to the obstructed vessel were excluded. The degree of stenosis (quantitative measurement of luminal obstruction) and total and regional left ventricular function were measured angiographically. Regional contractile reserve was determined from postextrasystolic angiograms. Ultrastructure and fibrotic content of the myocardium (morphometry) were determined from biopsy material taken at the time of bypass surgery from the area perfused by the left anterior descending artery. Graft flow to this artery was measured under basal conditions and after release of a 30 second graft occlusion (hyperemic response). Five groups were formed: I, no stenosis; II, stenosis of 50 to 79 percent; III, of 80 to 89 percent; IV, of 90 to 99 percent; and V, 100 percent occlusion. Patients in group II had normal values for ejection fraction, regional function and reserve, normal ultrastructure, a small degree of fibrosis and no hyperemic response after release of graft occlusion. Patients in group III had similar findings except for a significant hyperemic response. Patients in group IV had moderate depression of ejection fraction, regional function and reserve, moderate ultrastructural alterations, increased myocardial fibrosis and a high hyperemic response. Patients in group V had a severely impaired ejection fraction, absent regional function and reserve, severe cell alterations and extensive scar formation. Thus, a clear sequence of events occurs with progression of coronary stenosis: until 79 percent stenosis no significant reduction of mechanical function and myocardial structure occurs. With 80 to 89 percent stenosis, poststenotic vasodilation fully compensates for the stenosis as documented by normal mechanical function and normal myocardial structure. At 90 to 99 percent stenosis, vasodilatory compensation is inadequate: Regional function decreases, degenerative ultrastructural alterations appear and the fibrotic content of the myocardium increases. With complete occlusion, compensation is ineffective, and severe loss of function and extensive scars develop.

Hemodynamics alterations induced by isoproterenol and pacing after aortic valve replacement with the Björk-Shiley or St. Jude medical prosthesis.

Stress evaluation was carried out in 26 patients approximately 7 months after aortic valve replacement with Björk-Shiley valves (13 patients) and St. Jude medical valves (13 patients). During isoproterenol infusion (0.3 μg/kg/min), cardiac output increased by a factor of 1.5 and aortic valve area decreased by 50% for both valve groups, while transvalvular gradients (rest: 7 ± 2 vs 10 ± 5 mm Hg, p > 0.05) increased to 42 ± 18 vs 51 ± 18 mm Hg (p > 0.05), i.e., to levels of moderate aortic stenosis. However, during pacing stress these values progressively decreased with rising heart rates. In other postoperative evaluations that included ergometric stress with isoproterenol and pacing, induced hemodynamic changes after aortic valve replacement were predictable and consistent with regard to both direction and magnitude, and they differed characteristically according to the type of stress used.We conclude that no functional differences between Biork-Shiley and St. Jude medical valves can be claimed. Standardized evaluation with isoproterenol is a sensitive stress test of prosthetic valvular hemodynamics. Because of the apparent magnification of residual obstruction after aortic valve replacement, it has advantages over pacing.

Abolished compensation of cardiac performance after nitroglycerin in patients with ventricular asynergy

Summary Left ventricular function was studied in 40 patients before and 20 minutes after 1.6 mg. of sublingual nitroglycerin. Thirteen patients had no evidence of heart disease, 16 had obstructive coronary artery disease (85 per cent luminal narrowing) without ventricular asynergy and 11 had obstructive coronary artery disease with ventricular asynergy (as a consequence of prior transmural myocardial infarction). Before and after nitroglycerin end-diastolic volume, end-systolic volume, ejection fraction, and shortening of hemiaxes was comparable in the control group and in patients without asynergy. Before nitroglycerin end-diastolic volume, end-systolic volume and end-diastolic pressure were significantly elevated in patients with asynergy as compared to controls, while stroke volume was maintained within normal limits. Normally contracting segments in ventricles with asynergy showed a comparable percentage shortening of hemiaxes as was found in normal hearts. After nitroglycerin stroke volume was significantly reduced in asynergic ventricles as compared to both other groups. This was due to reduced shortening of normally contracting segments in ventricles with asynery, while shortening in asynergic areas remained unchanged after nitroglycerin. The results are explained on the basis of the Frank-Starling mechanism. An increased diastolic pressure is needed in enlarged hearts to enable noninfarcted myocardium to shorten. The result is a normal stroke volume. Nitroglycerin lowers diastolic pressure to that extent that shortening in noninfarcted segments is significantly reduced resulting in a fall of stroke volume. Since no improvement of left ventricular function could be demonstrated the beneficial effects of nitroglycerin are offset by the abolished compensation of cardiac output in ventricles with asynergy.

Cardiac reserve during isoproterenol stress in patients with aortic valve disease before and after corrective surgery

Abstract The relations between left ventricular (LV) hypertrophy as estimated by LV mass and LV function and between LV hypertrophy and cardiac reserve were evaluated in 26 patients with aortic valve disease and in nine normal patients who served as controls. Ejection fraction (EF) and mean circumferential fiber shortening rate (VCF) served as indices of LV function. Reserve force of the left ventricle was tested by ventriculography during infusion of 0.3 μg/Kg. body weight/min. isoproterenol. EF and VCF were not significantly different (p > 0.05) either at rest or during isoproterenol infusion if patients with aortic stenosis were compared to patients with aortic regurgitation having comparable LV masses. Therefore we correlated the EF and VCF to the LV mass of all patients irrespective of the type of aortic valve lesion. Poor but significant inverse correlations were found at rest between LV mass and EF (r = 0.62) and between LV mass and VCF (r = 0.57). These correlations improved considerably during isoproterenol: r = 0.84 for EF and r = 0.74 for VCF. LV function was evaluated in another six patients with aortic valve disease before and nine months after successful aortic valve replacement by Bjork-Shiley prostheses. LV mass before surgery was 3.6 times control and decreased after surgery to 1.7 times control (p

Hämodynamische Untersuchungen von Diprafenon mit der Conductance-Kathetertechnik und der schnellen Laständerung durch temporäre Ballonokklusion der Vena cava inferior

Kardiodepression bei der Diprafenon-Therapie ware ein unerwunschtes Nebenprodukt, zumal, wenn bereits eine eingeschrankte Myokardfunktion zugrunde lage, wie in der Mehrzahl der Falle. Ein negativer Einflus auf die linksventrikulare Pumpfunktion wird fur alle Klasse-I-Antiarrhythmika schon aufgrund ihres spezifischen Wirkungsmechanismus postuliert. Dabei bleibt aber unklar, ob die induzierten hamodynamischen Auswirkungen sich vorwiegend negativ inotrop, rein vasodilatatorisch oder in der Kombination dieser Wirkungen ausern. Da aber sowohl positiv inotrope als auch vasodilatatorisch wirksame Substanzen den Fullungsdruck und Gefaswiderstand senken und den Cardiac-Index steigern konnen, ergeben sich Schwierigkeiten bei der Unterscheidung der Reaktionsmuster von den Medikamentenwirkungen. Es war daher das Ziel dieser Untersuchung, akute diprafenoninduzierte hamodynamische Anderungen mit Hilfe ihrer endsystolischen Druck/Volumen-Beziehung zu analysieren. Dabei sah das Studiendesign vor, solche Wirkungen nicht nur unter Ruhebedingungen, sondern auch (der wirklichen klinischen Situation eher entsprechend) unter Tachykardie zu untersuchen.