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ABSTRACTS weeks after infarction, results in a 30% 1 year sur- vival rate, as published reports show. To date, surgical repair attempted within the first 2 weeks has been as- sociated with a prohibitively high mortality rate. At Stanford, 10 patients (age range 55-74 years) have undergone emergency surgical closure of the defect within an average of 8 days after infarction, and 5 days after the appearance of VSD. Each patient had refractory cardiogenic shock following the sudden onset of the typical findings of a VSD. The diagnosis was confirmed preoperatively by an oxygen step-up in the right ventricle. Surgical repair in each case involved closure of the defect with a Teflon@ patch supported in place by mattress sutures and Teflon felt pledgets, in addition to resection of an associated ventricular aneu- rysm in 2 patients. Five patients died within 1 week after surgery. The other 5 patients remain clinically well an average of 14 months (range 7-43 months) after surgery. Residual shunts are present in 2 pa- tients. This small series shows that successful surgical treatment of ventricular septal defects can be ac- complished within 2 weeks after infarction. The 1 year survival rate of 5O’/c compares favorably with the re- sults of elective repair of VSD’s occurring after infarc- tion. The Role of Platelet Aggregation in Catecholamine- Induced Cardiac Necrosis: Electron Microscopic and Drug Studies JACOB I. HAFT, MD*; KENNETH GERSHENGORN, MD; PAUL KRANZ. MD: FRANK ALBERT, MD; ROLF OESTREICHER, MD; KAZEM FANI, MD, New York, NewYork To determine if the cardiac necrosis seen after cate- cholamine infusion in experimental animals might be due to platelet aggregation in the capillaries of the heart (catecholamines cause platelet aggregation in vitro), studies (1) using drugs known to inhibit plate- let aggregation and (2) using electron microscopic methods were undertaken. In 1 study, 30 dogs were in- fused with epinephrine (4 pg/kg per min). Ten were pretreated with aspirin, 10 grains twice daily (A) for 4 days, 10 pretreated with dipyridamole, 50 mg twice daily (D), and 10 served as control dogs. All dogs had a significant increase in blood pressure during infu- sion. The dogs were killed 1 week later, and sections of the myocardium were studied histologically with necro- sis graded 0 to +++. All control dogs had cardiac ne- crosis; 5 +++, 3 ++ and 2 t. Seven of the 10 dogs treated with A and 7 of the 10 treated with D had no necrosis (P <O.Ol). One dog pretreated with D had ++, 1 had + and 1 trace necrosis; 3 dogs treated with A had + necrosis. In another study, 4 dogs were infused with norepinephrine, 4 pg/kg per min for 4 hours. At the end of the infusion they were killed, and cardiac sections were studied with the electron micro- scope. In all dogs capillaries were found that contained platelets adherent to the walls and to each other. Nu- merous capillaries were completely occluded by platelet thrombi with and without interspersed fibrin. The endothelium of the capillaries was damaged in some instances, but intact in others, thus suggesting that the aggregation of platelets was primary and not secon- dary to wall injury. It is concluded that platelet aggregation in capillaries plays a significant role in the production of cardiac necrosis by catecholamine infusion. This demonstra- tion that platelet aggregation can be induced in blood vessels by catecholamines in vivo raises the possibility that the relation between stress and coronary athero- sclerosis may be through catecholamine-induced aggre- gation of platelets on vascular endothelium serving as the nidus for the development of atherosclerotic plaques. Left Ventricular Function Following Successful Aortocoronary Vein Bypass GLEN W. HAMILTON. MD*; DOUGLAS K. STEWART, MD; KEN- NETH L. GOULD, MD; J. W. KENNEDY, MD, Seattle, Washington A previously published report suggested that success- ful aortocoronary vein bypass surgery is accompanied by improvement in left ventricular performance. This question was reexamined using standard hemodynamic and biplane angiocardiographic techniques. Pre- and postoperative results are available in 11 consecutive patients who had single (2)) double (9)) or triple (1) vein grafts which were patent at the time of restudy. After operation, angina was completely relieved in all patients. Values for left ventricular end-diastolic pres- sure (13 _t 5-11 t 6), end-diastolic volume (81 ? 17-77 -c- 12), stroke volume (44 2 12-39 c 9) and systolic ejection fraction (SEF) (55 -C 12-51 2 7) were not significantly changed after surgery. Neither patients with normal SEF (5) nor those with depressed SEF (6) demonstrated significant postoperative changes. We were unable to confirm an improvement in ventricular performance and believe that aortocoronary surgery preserves rather than improves ventricular perfor- mance. Alterations in Renal Vascular Resistance Following Coronary Artery Occlusion in Dogs HENRY G. HANLEY, MD*; ALBERT E. RAIZNER, MD; THOMAS V. INGLESBY. MD; NEWMAN S. SKINNER, Jr., MD, Atlanta, Georgia Since acute myocardial infarction with hypotension and cardiogenic shock appears to be infrequently associ- ated with acute tubular necrosis (ATN), accounting for only 19 of 1,731 cases of ATN in several large series, it seemed pertinent to study the behavior of the renal vascular bed during experimental coronary ar- tery occlusion (CAO). Both initial reflex responses and subsequent alterations in total renal vascular resis- tance (RVR) were evaluated (total 33 dogs) during CAO. An innervated, constant blood flow, perfused kid- ney preparation was used, which incorporated a delay circuit in the perfusion tubing so that any initial changes (up to 120 seconds) in RVR following CA0 could only be of reflex origin. In all animals, CA0 re- sulted in a mean decrease in systemic arterial pressure (SAP) of 27.8 r 2.3 “/o SEM. Despite this, the reflex re- sponse of the renal vascular bed was vasodilatation in 18 of 23 dogs. Mean RVR decreased 7.4 2 2.476 (P <0.005). CA0 was maintained for 11 or more minutes in 10 dogs. Reflex and persistent renal vasodilatation occurred in 7, whereas only 1 showed reflex and persis- tent vasoconstriction. The mean response of these 10 was persistent renal vasodilatation (P <0.05). In con- trast, hemorrhage for brief periods (10 dogs), result- ing in the same degree of decrease in SAP as CAO, was associated with an average increase in RVR of 268 The American Journal of CARDIOLOGY

The role of platelet aggregation in catecholamine-induced cardiac necrosis: Electron microscopic and drug studies

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ABSTRACTS

weeks after infarction, results in a 30% 1 year sur- vival rate, as published reports show. To date, surgical repair attempted within the first 2 weeks has been as- sociated with a prohibitively high mortality rate. At Stanford, 10 patients (age range 55-74 years) have undergone emergency surgical closure of the defect within an average of 8 days after infarction, and 5 days after the appearance of VSD. Each patient had refractory cardiogenic shock following the sudden onset of the typical findings of a VSD. The diagnosis was confirmed preoperatively by an oxygen step-up in the right ventricle. Surgical repair in each case involved closure of the defect with a Teflon@ patch supported in place by mattress sutures and Teflon felt pledgets, in addition to resection of an associated ventricular aneu- rysm in 2 patients. Five patients died within 1 week after surgery. The other 5 patients remain clinically well an average of 14 months (range 7-43 months) after surgery. Residual shunts are present in 2 pa- tients.

This small series shows that successful surgical treatment of ventricular septal defects can be ac- complished within 2 weeks after infarction. The 1 year survival rate of 5O’/c compares favorably with the re- sults of elective repair of VSD’s occurring after infarc- tion.

The Role of Platelet Aggregation in Catecholamine- Induced Cardiac Necrosis: Electron Microscopic and Drug Studies

JACOB I. HAFT, MD*; KENNETH GERSHENGORN, MD; PAUL KRANZ. MD: FRANK ALBERT, MD; ROLF OESTREICHER, MD; KAZEM FANI, MD, New York, NewYork

To determine if the cardiac necrosis seen after cate- cholamine infusion in experimental animals might be due to platelet aggregation in the capillaries of the heart (catecholamines cause platelet aggregation in vitro), studies (1) using drugs known to inhibit plate- let aggregation and (2) using electron microscopic methods were undertaken. In 1 study, 30 dogs were in- fused with epinephrine (4 pg/kg per min). Ten were pretreated with aspirin, 10 grains twice daily (A) for 4 days, 10 pretreated with dipyridamole, 50 mg twice daily (D), and 10 served as control dogs. All dogs had a significant increase in blood pressure during infu- sion. The dogs were killed 1 week later, and sections of the myocardium were studied histologically with necro- sis graded 0 to +++. All control dogs had cardiac ne- crosis; 5 +++, 3 ++ and 2 t. Seven of the 10 dogs treated with A and 7 of the 10 treated with D had no necrosis (P <O.Ol). One dog pretreated with D had ++, 1 had + and 1 trace necrosis; 3 dogs treated with A had + necrosis. In another study, 4 dogs were infused with norepinephrine, 4 pg/kg per min for 4 hours. At the end of the infusion they were killed, and cardiac sections were studied with the electron micro- scope. In all dogs capillaries were found that contained platelets adherent to the walls and to each other. Nu- merous capillaries were completely occluded by platelet thrombi with and without interspersed fibrin. The endothelium of the capillaries was damaged in some instances, but intact in others, thus suggesting that the aggregation of platelets was primary and not secon- dary to wall injury.

It is concluded that platelet aggregation in capillaries plays a significant role in the production of cardiac

necrosis by catecholamine infusion. This demonstra- tion that platelet aggregation can be induced in blood vessels by catecholamines in vivo raises the possibility that the relation between stress and coronary athero- sclerosis may be through catecholamine-induced aggre- gation of platelets on vascular endothelium serving as the nidus for the development of atherosclerotic plaques.

Left Ventricular Function Following Successful Aortocoronary Vein Bypass

GLEN W. HAMILTON. MD*; DOUGLAS K. STEWART, MD; KEN- NETH L. GOULD, MD; J. W. KENNEDY, MD, Seattle, Washington

A previously published report suggested that success- ful aortocoronary vein bypass surgery is accompanied by improvement in left ventricular performance. This question was reexamined using standard hemodynamic and biplane angiocardiographic techniques. Pre- and postoperative results are available in 11 consecutive patients who had single (2)) double (9)) or triple (1) vein grafts which were patent at the time of restudy. After operation, angina was completely relieved in all patients. Values for left ventricular end-diastolic pres- sure (13 _t 5-11 t 6), end-diastolic volume (81 ? 17-77 -c- 12), stroke volume (44 2 12-39 c 9) and systolic ejection fraction (SEF) (55 -C 12-51 2 7) were not significantly changed after surgery. Neither patients with normal SEF (5) nor those with depressed SEF (6) demonstrated significant postoperative changes. We were unable to confirm an improvement in ventricular performance and believe that aortocoronary surgery preserves rather than improves ventricular perfor- mance.

Alterations in Renal Vascular Resistance Following Coronary Artery Occlusion in Dogs

HENRY G. HANLEY, MD*; ALBERT E. RAIZNER, MD; THOMAS V. INGLESBY. MD; NEWMAN S. SKINNER, Jr., MD, Atlanta, Georgia

Since acute myocardial infarction with hypotension and cardiogenic shock appears to be infrequently associ- ated with acute tubular necrosis (ATN), accounting for only 19 of 1,731 cases of ATN in several large series, it seemed pertinent to study the behavior of the renal vascular bed during experimental coronary ar- tery occlusion (CAO). Both initial reflex responses and subsequent alterations in total renal vascular resis- tance (RVR) were evaluated (total 33 dogs) during CAO. An innervated, constant blood flow, perfused kid- ney preparation was used, which incorporated a delay circuit in the perfusion tubing so that any initial changes (up to 120 seconds) in RVR following CA0 could only be of reflex origin. In all animals, CA0 re- sulted in a mean decrease in systemic arterial pressure (SAP) of 27.8 r 2.3 “/o SEM. Despite this, the reflex re- sponse of the renal vascular bed was vasodilatation in 18 of 23 dogs. Mean RVR decreased 7.4 2 2.476 (P <0.005). CA0 was maintained for 11 or more minutes in 10 dogs. Reflex and persistent renal vasodilatation occurred in 7, whereas only 1 showed reflex and persis- tent vasoconstriction. The mean response of these 10 was persistent renal vasodilatation (P <0.05). In con- trast, hemorrhage for brief periods (10 dogs), result- ing in the same degree of decrease in SAP as CAO, was associated with an average increase in RVR of

268 The American Journal of CARDIOLOGY