Surgical intervention in acute myocardial infarction: an historical perspective.

Acute myocardial infarction is an evolving event that lends itself well to surgical intervention. An historical review of surgery of acute myocardial infarction, with specific emphasis on the Spokane data, shows that this can be done safely and efficiently with myocardial salvage. Those people who were operated on within 6 hours of the onset of symptoms of acute myocardial infarction had a clear reduction in hospital mortality incidence and a better long-term result. The conclusion of our review is that emergency coronary artery bypass grafting for acute evolving myocardial infarction should be considered as a therapeutic option in every patient. All other modalities of therapy should be compared with the results of acute bypass surgery.

Acute control of pulmonary regurgitation with a balloon "valve". An experimental investigation.

Operations for certain congenital cardiac lesions can produce pulmonary regurgitation. Pulmonary regurgitation contributes to right ventricular dysfunction, which may cause early postoperative morbidity and mortality. To ameliorate the problems of pulmonary regurgitation during the early postoperative period, we evaluated a method for its acute control. Complete pulmonary valvectomy was performed utilizing inflow occlusion in eight sheep. A catheter with a 15 ml spherical balloon was positioned in the pulmonary arterial trunk; its inflation and deflation were regulated by an intra-aortic balloon pump unit. Blood flow from the pulmonary arterial trunk and forward and regurgitant fraction were determined from electromagnetic flow transducer recordings. The regurgitant fraction with uncontrolled pulmonary regurgitation was 38% +/- 3% (forward flow = 42 +/- 5 ml/beat and regurgitant flow = 16 +/- 2 ml/beat). Inflation of the balloon during diastole was timed to completely eliminate pulmonary regurgitation. This balloon control of pulmonary regurgitation increased pulmonary arterial diastolic pressure from 12 +/- 1 to 17 +/- 1 mm Hg (p less than 0.0001) and decreased pulmonary arterial systolic pressure from 31 +/- 3 to 27 +/- 1 mm Hg (p = 0.06). Pulmonary arterial pulse pressure decreased from 19 +/- 3 to 9 +/- 1 mm Hg (p less than 0.003). Elimination of pulmonary regurgitation decreased right ventricular stroke volume (25 +/- 3 versus 42 +/- 5 ml/beat, p less than 0.0002) and resulted in a 46% reduction in right ventricular stroke work (5.0 +/- 0.6 versus 9.4 +/- 1.0 gm-m/beat, p less than 0.001) with no change in net forward pulmonary artery flow. Thus, acute pulmonary regurgitation can be controlled and this control improves overall hemodynamic status and decreases right ventricular work.

Pulmonary artery balloon counterpulsation for right ventricular failure. An experimental evaluation.

Right ventricular (RV) failure frequently occurs in patients undergoing correction of congenital cardiac defects, as well as in other clinical settings. RV hypertrophy was created in 10 neonatal lambs by pulmonary artery (PA) banding. Twelve months later RV hypertrophy was present (RV weight/body weight = 2.71 +/- 0.31 gm/kg); RV systolic pressures were elevated (65 +/- 9 mm Hg) and the average gradient across the PA band was 38 +/- 9 mm Hg. RV failure was produced in all animals by performing a right ventriculotomy. Four unassisted (control) animals died shortly after separation from bypass. Six experimental animals underwent pulmonary artery balloon counterpulsation (PABCP). A Dacron graft anastomosed to the proximal PA served as a reservoir for a 40 ml intra-aortic balloon pump system. PABCP effectively reversed RV failure, low cardiac output, and systemic arterial hypotension. Periods with PABCP on and off in each animal were compared. PABCP increased cardiac output from 1.45 +/- 0.16 to 2.03 +/- 0.13 L/min (p less than 0.0001) and increased aortic systolic pressure from 78 +/- 7 to 99 +/- 6 mm Hg (p less than 0.0004). PABCP produced a significant reduction in RV peak systolic pressure from 56 +/- 5 to 41 +/- 3 mm Hg (p less than 0.0001). PA peak pressure distal to the band increased from 31 +/- 2 to 40 +/- 1 mm Hg (p less than 0.0001). Right atrial pressure decreased from 14 +/- 1 to 11 +/- 1 mm Hg (p less than 0.0001) with PABCP, and RV end-diastolic pressure fell from 15 +/- 1 to 11 +/- 1 mm Hg (p less than 0.0001). RV stroke work index increased 49% from 0.081 +/- 0.011 to 0.121 +/- 0.017 gm X m/kg/beat (p less than 0.01), and RV systolic pressure time index decreased 38% from 1140 +/- 79 to 710 +/- 65 mm Hg sec/min (p less than 0.0001). Thus PABCP in the presence of RV dysfunction can produce substantial improvement in RV function and in overall cardiac function and may prove clinically useful in managing patients in refractory RV failure.

Effect of intrarenal administration of dopamine on renin release in conscious dogs.

We investigated the effect of intrarenal administration of dopamine on renin release in conscious dogs. Dopamine in doses ranging from 0.28 to 3.0 micrograms . kg(-1) . min(-1) produced a significant increase in systemic plasma renin activity (PRA) and renin secretion rate without altering systemic blood pressure. Dopamine also induced renal vasodilatation and natriuresis within this dose range. To determine if the dopamine-induced renin release is related to its vasodilatory action, two other vasodilators, papaverine and acetylcholine, were infused into the renal artery, but neither, in doses that produced a rise in renal blood flow similar to that of dopamine, had any effect on PRA. As dopamine can activate alpha- and beta-adrenergic receptors in addition to dopaminergic receptors, experiments were also performed to characterize the type of receptors involved in dopamine-induced renin release. Intrarenal infusion of sulpiride and haloperidol, dopamine antagonists, significantly inhibited dopamine-induced renin release and renal vasodilatation. In contrast, intrarenal infusion of propranolol failed to alter dopamine-induced rise in PRA or renal blood flow. Simultaneous infusion of phentolamine and dopamine, on the other hand, produced a significant potentiation of dopamine-induced renin release and renal vasodilatation. In conclusion, our studies demonstrate that dopamine is capable of inducing renin release and renal vasodilatation in conscious dogs. Moreover, such actions of dopamine are mediated through activation of specific dopamine receptors in the kidney. Finally, we present evidence for the existence of the intrarenal alpha-adrenergic mechanism that is inhibitory to renin release.

Mitral valve replacement after closed mitral commissurotomy.

Closed mitral commissurotomy (CMC) was performed at the National Heart Institute in 303 patients (73% women, 27% men; mean age 40 years) with acquired isolated mitral stenosis between 1954 and 1980. The average mean mitral valve gradient decreased from 14.2 +/- 0.4 to 5.3 +/- 0.4 mm Hg (p less than 0.001), and mitral valve area index increased from 0.7 +/- 0.03 to 1.4 +/- 0.9 cm2/m2 (p less than 0.001). The perioperative mortality was 2%. Ninety-two percent of patients improved one or more functional classes after CMC. Actuarial survival was 95%, 82% and 70% at 5, 10 and 15 years after CMC, respectively. Fifty-four patients (18%) required mitral valve replacement (MVR) a mean of 9.6 years after commissurotomy (range 1-26 years). Before CMC, factors associated with later MVR included preoperative functional class, calcification of the mitral valve, and the absence of an opening snap. After CMC, poor functional improvement, congestive heart failure, atrial fibrillation, and the necessity for a repeat CMC were associated with late MVR. Catheterization after CMC showed that patients who later required MVR had a smaller decrease in left atrial pressure (p less than 0.001), more mitral regurgitation (p less than 0.001), and were more likely to have pulmonary hypertension (p less than 0.05). The indications for MVR were residual stenosis with or without mild mitral regurgitation in 33 patients (61%), restenosis in 15 (28%), and moderate-to-severe regurgitation in six (11%). Perioperative mortality for valve replacement was 13%. Among survivors, 88% improved at least one functional class after valve replacement. Actuarial survival was estimated to be 95% at 5 years and 74% at 10 years after MVR. This study confirms that CMC provides excellent long-term hemodynamic and clinical improvement in appropriately selected patients. When symptomatic deterioration occurs late after CMC, MVR restores clinical and hemodynamic improvement in many patients. CMC continues to be performed at the National Heart Institute in selected patients with acquired mitral stenosis.

Sequential renal hemodynamics in experimental benign and malignant hypertension.

To examine the sequential renal hemodynamic changes in experimental renovascular hypertension, the uninephrectomized dog was studied immediately after renal artery constriction, throughout chronic benign hypertension, and during malignant hypertension. Intrarenal resistance fell immediately after renal artery constriction, but rose above control within hours. Intrarenal infusion of teprotide resulted in vasodilatation during the first 3 days but failed to do so during the chronic phase of benign hypertension. During the transition from benign to malignant hypertension, angiotensin II-dependent renal vasoconstriction developed associated with natriuresis, plasma volume contraction and a vicious cycle of hyperreninemia and severe vascular damage.

Influence of dietary sodium on renin activity and arterial pressure during anesthesia.

The effect of pentobarbital anesthesia on plasma renin activity (PRA) and mean arterial pressure (MAP) was studied in chronically catheterized dogs maintained on normal or low-sodium intake. Within 1 min of administration, pentobarbital caused a rapid fall in MAP which was followed by a restoration of MAP toward control within 5 min. Thirty minutes after induction of anesthesia, PRA was unchanged in sodium-replete dogs and elevated two-fold in sodium-depleted dogs. MAP was significantly lowered (20 mmHg) in normal salt dogs and only slightly decreased in low-salt dogs 30 min after pentobarbital. MAP returned to preanesthetic control value in dogs given converting enzyme inhibitor before anesthesia. Surgical stress or cutaneous electrical stimulation causey hexamethonium. These results indicate that change in PRA and MAP of pentobarbital-anesthetized dogs is significantly influenced by the sodium intake of the animal and by the degree of surgical stress.