F Schwarz

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.

Reduced volume fraction of myofibrils in myocardium of patients with decompensated pressure overload.

The relation between quantitative ultrastructural changes of the left ventricular (LV) myocardium and contractile function was studied in patients with chronic aortic stenosis (AS). The volume fractions of myofibrils, sarcoplasm and mitochondria in myocardial cells were determined by electron microscopic morphometry in small LV tissue samples of 19 patients with AS. Interstitial fibrosis was measured by light microscopic morphometry. Transmural biopsies of the LV free wall perfused by the anterior descending branch of the left anterior descending coronary artery (LAD) were obtained during aortic valve replacement. LV function was analyzed from preoperative right- and left-heart catheterization and angiography. Group 1 consisted of seven patients with ejection fractions (EFs) greater than 55% and mean left atrial pressure (LAP) less than 15 mm Hg. Group 2 consisted of 12 patients with EFs less than 55% and mean LAP greater than 15 mm Hg. Patients in group 1 had lower LV end-diastolic volume (91.9 vs 145.3 ml/m2, p < 0.05) and lower LV muscle mass (148.3 vs 199.8 g/m2, p < 0.05) than patients in group 2. The volume fraction of myofibrils was higher in group 1 than in group 2 (48.4 vs 42.1%, p < 0.05), while volume fractions of sarcoplasm (31.7 vs 36.0%) and mitochondria (20.9 vs 22.0%) were comparable (p > 0.05). Interstitial myocardial fibrosis did not differ between groups (16.3 vs 14.7%, p > 0.05). Biopsies from the area perfused by the LAD in 10 additional surgical patients who had coronary artery disease with moderate LAD stenosis and normal wall motion in the area of LV free wall perfused by the LAD were taken as controls for morphometric data. No significant difference of ultrastructural data was found between group 1 and controls. The volume fraction of myofibrils was lower in group 2 than in controls (42.1 vs 52.9%, p < 0.001), and the volume fraction of sarcoplasm was higher (36.0 vs 21.1%, p < 0.001). Mitochondria and interstitial fibrosis did not differ in group 2 and controls (p > 0.05).Thus, intracellular reduction in the volume fraction of myofibrils was the major morphologic finding in LV biopsy samples of patients with decompensated pressure overload.

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.

Native collaterals in the development of collateral circulation after chronic coronary stenosis in mongrel dogs.

The response of native collateral circulation to chronic stenosis of the left circumflex coronary artery (LCx) was studied in 17 mongrel dogs. Stenosis restricted reactive hyperemia of the LCx without affecting resting flow. Regional myocardial blood flow was measured by the tracer microsphere technique. Coronary collateral blood flow to the LCx was determined during maximal reactive hyperemia of the left anterior descending branch before and 5 weeks after implantation of a fixed LCx stenosis in the open‐chest preparation. The protective effect of collaterals was tested by LCx ligation 5 weeks after implantation of stenosis. Presence of acute myocardial infarction was determined by nitroblue tetrazolium staining. Eleven dogs had a myocardial infarction (group A), but six dogs showed no evidence of infarction at autopsy (group B). In group A, collateral flow and minimal coronary resistance of the LCx bed changed little after LCx stenosis, from 12 to 15 ml/min/100 g and from 10.5 to 10.0 mm Hg/ml/min/100 g, respectively (both p > 0.05). In contrast, collateral flow in group B increased from 22 to 102 ml/min/100 g (p < 0.05), and minimal coronary resistance of the LCx bed decreased from 4.8 to 1.4 mm Hg/ml/min/100 g (p < 0.01). Group A had lower native collateral flow (p < 0.05) and higher native minimal coronary resistance of the LCx bed than group B (p < 0.05). Postobstructive LCx pressure correlated well with blood flow data. The LCx risk region was of comparable size in groups A and B, 36.4% vs 39.0% of total left ventricle (p > 0.05). Two responses of collateral circulation to chronic stenosis were documented: lack of collateral growth in group A, but significant collateral growth in group B. The natural variation of collateral circulation was the major determinant of the different responses that were important with stenosis of a major coronary artery.

Coronary collateral vessels: Their significance for left ventricular histologic structure

Whether coronary collateral vessels protect the left ventricular myocardium is unknown. Light microscopic morphometry was carried out on myocardial tissue samples from 56 surgically treated patients with coronary artery disease. Transmural biopsy of the myocardium perfused by the left anterior descending coronary artery was obtained during open heart surgery. In initial reproducibility studies of biopsy samples of 17 patients a sampling error for evaluation of myocardium was defined and differences in transmural fibrosis exceeding +/- 6.2 percent were considered biologically significant. Stenosis of the left anterior descending artery was determined from preoperative angiography. Group A (control group) comprised patients with less than 75 percent area reduction of the left anterior descending coronary artery (mean +/- standard deviation 65 +/- 10 percent). Patients in group B (more than 95 percent area reduction [mean 99 +/- 2 percent] without collateral supply on arteriography) were compared with patients in group C (identical stenosis [mean 99 +/- 2 percent] but with collateral supply). Fibrosis averaged 17 percent in group A, 68 percent in group B (p less than 0.001 versus group A) and 29 percent in group C (p greater than 0.05 versus group A, p less than 0.001 versus group B). Thus, in severe coronary stenosis myocardium supplied by collateral vessels shows less fibrosis on biopsy sample than does myocardium without collateral supply.

Functional significance of coronary collaterals in man

SummaryIn 29 patients with coronary artery disease the functional significance of coronary collaterals was studied during surgery for aortocoronary bypass grafting.Poststenotic coronary pressure and postocclusion graft flow hyperemia were measured in 34 vessels receiving a coronary bypass graft. The vessels were divided into groups according to the angiographically determined degree of coronary stenosis: group I: stenosis up to 80%, group II: stenosis between 80 and 90%, group III: stenosis between 90 and 100%, Group IV: acute occlusion without visible collaterals and Group V: complete occlusions with collaterals. When a coronary stenosis surpasses 80% luminal narrowing it becomes hemodynamically significant: pressure gradient over the stenosis becomes significant and there appears a hyperemic response after graft occlusion. From group I to IV poststenotic coronary pressure decreases and graft flow hyperemia increases significantly (p<0.05).In all cases general coronary vasodilation was produced by intracoronary injection of dipyridamole. After vasodilation poststenotic coronary pressure decreased significantly (p<0.05) in groups I and II but not in III and IV. This indicates that there is still some increase in flow over the stenosis i.e. coronary reserve is not completely expended until 90% stenosis. Hyperemic graft flow response correlates well with poststenotic coronary pressure: the relation can be described by an asymptotic regression. This suggests that graft flow hyperemia is a reflection of compensatory peripheral vasodilation rather than a response to ischemia.In group V, i.e. complete chronic occlusions with collaterals, peripheral coronary pressure was 40.7±3.3% of systemic pressure and this value decreased significantly (p=0.002) to 34.0±2.6% after vasodilation. Hyperemic response was 1.57±0.07. These values are significantly different from groups I and IV, but not from II and III.These findings suggest that coronary collaterals restore coronary reserve partially. Nevertheless, a chronic coronary occlusion compensated by collaterals corresponds functionally to a 90% pure stenosis.ZusammenfassungDie Bedeutung des koronaren Kreislaufes wurde an 29 Patienten mit koronarer Herzerkrankung während der aortokoronaren Bypassoperation untersucht. Poststenotischer Koronararteriendruck und Graftfluß vor und 30 sec nach Graftverschluß wurden an 34 Gefäßen, die mit einem aortokoronaren Bypass versorgt wurden, gemessen. Nach dem angiografisch bestimmten Grad der Koronararterienstenose (% Lumeneinengung) wurden folgende Gruppen gebildet: Gruppe I = Stenose bis 80%, Gruppe II = Stenose zwischen 80 und 90%. Gruppe III = Stenose zwischen 90 und 100%, Gruppe IV = akuter Verschluß ohne angiographisch sichtbare Kollateralen und Gruppe V = kompletter Verschluß mit Kollateralen. Wenn eine Koronarstenose 80% Lumeneinengung erreicht, wird sie hämodynamisch bedeutsam, es entsteht ein signifikanter Druckgradient über die Stenose und eine signifikante Hyperämie nach Öffnen des Grafts. Von Gruppe I bis IV fand sich ein signifikanter Abfall des poststenotischen Druckes und ein signifikanter Anstieg des hyperämischen Graftflusses. Maximale koronare Vasodilatation wurde durch Injektion von Dipyridamol in den Graft induziert. Der poststenotische Druck fiel nach Vasodilatation signifikant ab in Gruppe I und II, nicht in III und IV. Dies bedeutet, daß unter 90% Stenose immer noch der Fluß über die Stenose gesteigert werden kann, die Koronar-reserve ist nicht völlig aufgebraucht. Eine signifikante asymptotische Relation besteht zwischen hyperämischem Graftfluß und poststenotischem Druck. Dies weist darauf hin, daß die hyperämische Reaktion nach Graftverschluß ein Maß der poststenotischen Vasodilatation ist und nicht ein Zeichen von Ischämie. In Gruppe V (kompletter Verschluß mit Kollateralen) war der poststenotische Druck 40,7±3,3% des systemischen Druckes, und dieser Wert fiel signifikant auf 34,0±2,6% nach Vasodilation ab. Die Hyperämie nach Öffnen des Grafts betrug 1,57±0,07 des Kontrollflusses. Diese Werte sind signifikant unterschiedlich von Gruppe I und IV, nicht von II und III.Wir schließen daraus, daß koronare Kollateralen die Koronarreserve teilweise wiederherstellen. Ein chronischer Koronarverschluß mit Kollateralen entspricht funktionell einer 90%igen Koronarstenose ohne Kollateralen.

Coronary collaterals in the canine heart: development and functional significance.

Abstract The development and functional significance of coronary collaterals was studied using the tracer microspheres technique in 18 mongrel dogs with complete chronic occlusion of the left circumflex coronary artery. In a first group of eight dogs resistance of the preexisting collaterals was determined during short acute occlusion of the left circumflex coronary artery (LC). The mean value was 8.49 resistance units (R.U.). Six weeks after the implantation of an Ameroid constrictor on the LC, collateral resistance decreased significantly (p In the second group of 10 animals no myocardial infarction was found six weeks after Ameroid constrictor implantation. In this group a stress test was performed by infusion of norepinephrine intravenously. In the areas perfused by normal coronary arteries, there was a significant relation between myocardial blood flow (MBF) and pressure-rate product (PRP). The collateralized subendocardium, however, failed to raise its blood flow with increasing PRP. After bypass to the occluded LC, the normal MPF-PRP relation was restored. These observations indicate that a significant collateral circulation develops after chronic coronary obstruction and protects the myocardium against infarction in most cases. The functional capacity of these collaterals, however, is limited and becomes inadequate under stress conditions.

Tolerance to ischemia of hypertrophied human hearts during valve replacement.

SummaryThis study evaluates the tolerance to ischemia during induced cardiac arrest in patients undergoing aortic valve replacement. In all patients cardiac standstill was of 45 minutes duration. Biopsies for electron microscopic study were taken from the left ventricle before induction of arrest, at the end of the ischemic period and 20 minutes after coronary perfusion had been reestablished. Structural ischemic damage was more pronounced in patients with severe hypertrophy and structural reconstitution was delayed. Degenerative changes of the myocardial cells, although observed frequently, apparently did not influence the tolerance to ischemia. It is concluded from this study that patients with severe hypertrophy represent a high-risk group in cardiac surgery because of their reduced tolerance to induced myocardial ischemia during cardiopulmonary bypass.ZusammenfassungWir untersuchten in dieser Arbeit die Ischämietoleranz hypertrophierter Herzen bei künstlich induziertem Herzstillstand während Operationen in totalem kardiopulmonalem Bypass. Bei allen Patienten dauerte der Herzstillstand 45 Minuten. Für die elektronenmikroskopische Untersuchung wurden Biopsien aus dem linken Ventrikel zu folgenden Zeitpunkten entnommen: vor der Einleitung des Herzstillstandes, am Ende des ischämischen Intervalls und 20 Minuten nach Wiederherstellung der Koronarperfusion.Die feinstrukturelle Beschädigung des Myokards, verursacht durch die Ischämie, nahm zu mit dem Schweregrad der Hypertrophie, desgleichen war die Wiederherstellung der strukturellen Schäden verzögert bei stärkerer Hypertrophie.Die häufig vorhandenen degenerativen Veränderungen im Herzmuskel beeinflußten die Ischämietoleranz nicht.Aus diesen Resultaten ergibt sich, daß Patienten mit kardialer Hypertrophie mittleren bis schweren Grades eine Risikogruppe für die Herzchirurgie darstellen, da ihre Ischämietoleranz eingeschränkt ist.This study evaluates the tolerance to ischemia during induced cardiac arrest in patients undergoing aortic valve replacement. In all patients cardiac standstill was of 45 minutes duration. Biopsies for electron microscopic study were taken from the left ventricle before induction of arrest, at the end of the ischemic period and 20 minutes after coronary perfusion had been reestablished. Structural ischemic damage was more pronounced in patients with severe hypertrophy and structural reconstitution was delayed. Degenerative changes of the myocardial cells, although observed frequently, apparently did not influence the tolerance to ischemia. It is concluded from this study that patients with severe hypertrophy represent a high-risk group in cardiac surgery because of their reduced tolerance to induced myocardial ischemia during cardiopulmonary bypass. Wir untersuchten in dieser Arbeit die Ischämietoleranz hypertrophierter Herzen bei künstlich induziertem Herzstillstand während Operationen in totalem kardiopulmonalem Bypass. Bei allen Patienten dauerte der Herzstillstand 45 Minuten. Für die elektronenmikroskopische Untersuchung wurden Biopsien aus dem linken Ventrikel zu folgenden Zeitpunkten entnommen: vor der Einleitung des Herzstillstandes, am Ende des ischämischen Intervalls und 20 Minuten nach Wiederherstellung der Koronarperfusion. Die feinstrukturelle Beschädigung des Myokards, verursacht durch die Ischämie, nahm zu mit dem Schweregrad der Hypertrophie, desgleichen war die Wiederherstellung der strukturellen Schäden verzögert bei stärkerer Hypertrophie. Die häufig vorhandenen degenerativen Veränderungen im Herzmuskel beeinflußten die Ischämietoleranz nicht. Aus diesen Resultaten ergibt sich, daß Patienten mit kardialer Hypertrophie mittleren bis schweren Grades eine Risikogruppe für die Herzchirurgie darstellen, da ihre Ischämietoleranz eingeschränkt ist.

Hypertrophic and Degenerative Changes of the Myocardium and the Influence of Ischemia During Cardiac Surgery

In a previous study [3] ultrastructural changes occurring in human myocardial tissue during ischemia and during reperfusion after ischemia were investigated in order to evaluate the tolerable duration of induced cardiac arrest during open-heart surgery. It was concluded that 45 min of ischemia resulted in a moderate degree of myocardial damage and a relatively fast recovery of the tissue structure during reperfusion of the heart. However, tolerance to ischemia as indicated by ultrastructural changes was not the same in all patients.

Quantitative ultrastructure of the myocardium in chronic aortic valve disease@@@Quantitative ultrastrukturelle Befunde des Myokards bei Patienten mit chronischen Aortenklappenvitien

SummaryLight and electron microscopic morphometry was carried out in tissue samples which were obtained from the left ventricular free wall in 29 patients with chronic aortic valve disease during open-heart surgery. 6 patients had aortic stenosis, 9 had aortic insufficiency and 14 had a mixed aortic valve lesson. Hemodynamics were studied before operation. Patients with mixed aortic valve disease had a higher left ventricular mass, a lower ejection fraction and mean circumferential fiber shortening rate than patients with aortic stenosis. Peak systolic wall stress was comparable between groups. The intracellular content of contractile material was lower and the sarcoplasmic volume was higher in mixed aortic valve disease than in aortic stenosis. Mitochondrial volume and interstitial fibrosis were not different between groups. Patients with aortic insufficiency showed no significant difference of parameters as compared to both other groups. We conclude that an intracellular deficiency of myofibrils causes lack of contractility in advanced hypertrophy due to mixed aortic valve disease.ZusammenfassungLicht- und elektronenoptische Morphometrie wurde an Gewebeproben des linken Ventrikels durchgeführt, die bei der Herzoperation entnommen wurden. 6 Patienten hatten eine Aortenstenose, 9 eine Aorteininsuffizienz und 14 ein kombiniertes Aortenvitium. Hämodynamische Messungen wurden vor der Operation durchgeführt. Patienten mit kombiniertem Aortenvitium hatten eine höhere linksventrikuläre Masse, eine niedrigere Ejektionsfraktion und Verkürzungsgeschwindigkeit als Patienten mit Aortenstenose. Der systolische “Wall Stress” war vergleichbar in den 3 Gruppen. Der intrazelluläre Gehalt an Myofibrillen war geringer, und der sarkoplasmatische Raum war höher bei kombinierten Aortenvitien als bei Aortenstenose. Das Mitochondrienvolumen und die interstitielle Fibrose waren nicht unterschiedlich in den Gruppen. Patienten mit Aorteninsuffizienz zeigten keinen signifikanten Unterschied zu den beiden anderen Gruppen. Wir schließen daraus, daß eine intrazelluläre Verarmung von kontraktilem Material die Ursache der eingeschränkten Myokardfunktion bei fortgeschrittener Hypertrophie infolge kombinierten Aortenvitiums ist.