Background. Left ventricular dilatation and dysfunction after myocardial infarction are major predictors of death. In experimental and clinical studies, long-term therapy with the angiotensin-converting—enzyme inhibitor captopril attenuated ventricular dilatation and remodeling. We investigated whether captopril could reduce morbidity and mortality in patients with left ventricular dysfunction after a myocardial infarction. Methods. Within 3 to 16 days after myocardial infarction, 2231 patients with ejection fractions of 40 percent or less but without overt heart failure or symptoms of myocardial ischemia were randomly assigned to receive double-blind treatment with either placebo (1116 patients) or captopril (1115 patients) and were followed for an average of 42 months. Results. Mortality from all causes was significantly reduced in the captopril group (228 deaths, or 20 percent) as compared with the placebo group (275 deaths, or 25 percent); the reduction in risk was 19 percent (95 percent conf...

Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. results of the survival and ventricular enlargement trial

An acute myocardial infarction, particularly one that is large and transmural, can produce alterations in the topography of both the infarcted and noninfarcted regions of the ventricle. This remodeling can importantly affect the function of the ventricle and the prognosis for survival. In the early period, infarct expansion has been recognized by echocardiography as a lengthening of the noncontractile region. The noninfarcted region also undergoes an important lengthening that is consistent with a secondary volume-overload hypertrophy and that can be progressive. The extent of ventricular enlargement after infarction is related to the magnitude of the initial damage to the myocardium and, although an increase in cavity size tends to restore stroke volume despite a persistently depressed ejection fraction, ventricular dilation has been associated with a reduction in survival. The process of ventricular enlargement can be influenced by three interdependent factors, that is, infarct size, infarct healing, and ventricular wall stresses. A most effective way to prevent or minimize the increase in ventricular size after infarction and the consequent adverse effect on prognosis is to limit the initial insult. Acute reperfusion therapy has been consistently shown to result in a reduction in ventricular volume. The reestablishment of blood flow to the infarcted region, even beyond the time frame for myocyte salvage, has beneficial effects in attenuating ventricular enlargement. The process of scarification can be interfered with during the acute infarct period by the administration of glucocorticosteroids and nonsteroidal antiinflammatory agents, which result in thinner infarcts and greater degrees of infarct expansion. Modification of distending or deforming forces can importantly influence ventricular enlargement. Even short-term augmentations in afterload have deleterious long-term effects on ventricular topography. Conversely, judicious use of nitroglycerin seems to be associated with an attenuation of infarct expansion and long-term improvement in clinical outcome. Long-term therapy with an angiotensin converting enzyme inhibitor can favorably alter the loading conditions on the left ventricle and reduce progressive ventricular enlargement as demonstrated in both experimental and clinical studies. With the former therapy, this attenuation of ventricular enlargement was associated with a prolongation in survival. The long-term clinical consequences of long-term angiotensin converting enzyme inhibitor therapy after myocardial infarction is currently being evaluated. Although studies directed at attenuating left ventricular remodeling after infarction are in the early stages, it does seem that this will be an important area in which future research might improve long-term outcome after infarction.

Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications.

Left ventricular remodeling is a major cause of progressive heart failure and death after myocardial infarction. Although neoangiogenesis within the infarcted tissue is an integral component of the remodeling process, the capillary network is unable to support the greater demands of the hypertrophied myocardium, resulting in progressive loss of viable tissue, infarct extension and fibrous replacement. Here we show that bone marrow from adult humans contains endothelial precursors with phenotypic and functional characteristics of embryonic hemangioblasts, and that these can be used to directly induce new blood vessel formation in the infarct-bed (vasculogenesis) and proliferation of preexisting vasculature (angiogenesis) after experimental myocardial infarction. The neoangiogenesis resulted in decreased apoptosis of hypertrophied myocytes in the peri-infarct region, long-term salvage and survival of viable myocardium, reduction in collagen deposition and sustained improvement in cardiac function. The use of cytokine-mobilized autologous human bone-marrow-derived angioblasts for revascularization of infarcted myocardium (alone or in conjunction with currently used therapies) has the potential to significantly reduce morbidity and mortality associated with left ventricular remodeling.

Neovascularization of ischemic myocardium by human bone-marrow–derived angioblasts prevents cardiomyocyte apoptosis, reduces remodeling and improves cardiac function

Surgical repair of tricuspid atresia has been carried out in three patients; two of these operations have been successful. A new surgical procedure has been used which transmits the whole vena caval blood to the lungs, while only oxygenated blood returns to the left heart. The right atrium is, in this way, `ventriclized', to direct the inferior vena caval blood to the left lung, the right pulmonary artery receiving the superior vena caval blood through a cava-pulmonary anastomosis. This technique depends on the size of the pulmonary arteries, which must be large enough and at sufficiently low pressure to allow a cava-pulmonary anastomosis. The indications for this procedure apply only to children sufficiently well developed. Younger children or those whose pulmonary arteries are too small should be treated by palliative surgical procedures.

https://thorax.bmj.com/content/thoraxjnl/26/3/240.full.pdf

Surgical repair of tricuspid atresia

Impairment of left ventricular function is the major predictor of mortality after acute myocardial infarction, but it is not known whether this is best described by ejection fraction or by end-systolic or end-diastolic volume. We measured volumes, ejection fractions, and severity of coronary arterial occlusions and stenoses in 605 male patients under 60 years of age at 1 to 2 months after a first (n = 443) or recurrent (n = 162) myocardial infarction and followed these patients for a mean of 78 months for survivors (range 15 to 165 months). There were 101 cardiac deaths, 71 (70%) of which were sudden (instantaneous or found dead). Multivariate analysis with log rank testing and the Cox proportional hazards model showed that end-systolic volume (chi 2 = 82.9) had greater predictive value for survival than end-diastolic volume (chi 2 = 59.0) or ejection fraction (chi 2 = 46.6), whereas stepwise analysis showed that once the relationship between survival and end-systolic volume had been fitted, there was no additional significant predictive information in either end-diastolic volume or ejection fraction. Severity of coronary occlusions and stenoses showed additional prediction of only borderline significance (p = .04 in one analysis), but continued cigarette smoking did remain an independent risk factor after stepwise analysis. For a subset of patients (n = 200) who had taken part in a randomized trial of coronary artery surgery after recovery from infarction, surgical "intention to treat" showed no predictive value.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction.

Factors associated with total cardiac mortality, sudden cardiac death and reinfarction were studied in 325 male survivors aged younger than 60 years of age (mean 50) of a first myocardial infarction (MI). All patients had undergone exercise testing and cineangiocardiography 4 weeks after MI, 24% underwent coronary artery surgery and 30% received β-blocking therapy. Patients were followed 1 to 6 years (mean 3.5). Total cardiac mortality was best predicted by the left ventricular (LV) ejection fraction (EF) and by a coronary prognostic index. In contrast, neither the severity of coronary arterial lesions measured with a scoring system nor the results of the exercise test gave significant prediction of mortality. Of the 2 major late sequelae of MI, reinfarction could not be predicted by any clinical or cineangiocardiographic variable. However, sudden death not associated with reinfarction was significantly more common (p 40%. Comparison of patients with an EF It is concluded that, at least for groups of patients treated with standard modern methods after MI, the main determinant of medium-term survival is the extent of LV damage. The state of the coronary arteries and the presence of ischemic myocardium during exercise are only of secondary importance for survival.

Prognosis after recovery from first acute myocardial infarction: Determinants of reinfarction and sudden death☆

Five cases of anomalous origin of the left main (LM) coronary artery from the right anterior aortic sinus are presented. In 4 patients the anomalous artery ran a septal course through the floor of the right ventricular infundibulum and in 1 an interarterial course between the aorta and pulmonary trunk. The cineangiographic features of these courses are contrasted with arteries running anterior free wall and retro-aortic courses. A caudal anterior loop of the anomalous LM coronary artery indicates a septal course, a cranial posterior loop an interarterial course, a cranial anterior loop an anterior free wall course and a caudal posterior loop a retro-aortic course. Review of previously documented cases shows that the septal course is relatively common, although previously not recognized.

Anomalous origin of the left main coronary artery from the right anterior aortic sinus: angiographic definition of anomalous course

An initial series of 101 patients with a homograft aortic valve has been reviewed from 4 to 6 years postoperatively. There were six hospital and 24 late deaths, eight of which were due to homograft valve failure. The 71 surviving patients were all symptomatically improved. Anticoagulants were not used, and emboli were thought not to originate from the valve.

Important incompetence occurred in 27 patients and reoperation was undertaken in 17 of these. The causes were peripheral leaking of the suture line, cusp rupture, bacterial endocarditis, and valve misplacement.

Leaflet calcification produced stenosis, requiring reoperation in two patients, and was significant in eight other valves. Precipitating causes, present in eight of the 10 cases, were imperfections in the original homograft, valve misplacement, or endocarditis.

Both cusp rupture and leaflet calcification were related to the method of valve preparation as neither was encountered in untreated valves. For this reason, chemical sterilization and freeze drying have been replaced by sterilization and storage in an antibiotic Hank's solution.

Aortic Homograft Valve Replacement A Long-Term Follow-Up of an Initial Series of 101 Patients

Prosthetic material was used in the repair of coarctation of the aorta in 72 patients followed for 8 months to 24 years after operation. False aneurysms occurred late postoperatively in 1 of 17 instances when a tube graft was used to replace the resected aorta and in 1 of 2 patients when the graft bypassed the obstructed area. A Dacron® onlay patch graft (DOPG) was used in 52 patients as the primary method of repair, to revise a previous repair or as an adjunct to another procedure at the time of initial operation. True of false late aneurysm occurred between 6 and 18 years postoperatively in 5 of the 38 patients in whom a DOPG was used for primary repair of the coarctation or to revise an earlier repair, an actuarial incidence of 38% at 14 years. Diagnosis of aneurysm formation late post-operatively depends on awareness of this complication and careful assessment of lateral as well as posteroanterior chest radiographs. DOPG should be avoided whenever possible.

Peter W.T. Brandt

Papers

Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction.

Prognosis after recovery from first acute myocardial infarction: Determinants of reinfarction and sudden death☆

Anomalous origin of the left main coronary artery from the right anterior aortic sinus: angiographic definition of anomalous course

Aortic Homograft Valve Replacement A Long-Term Follow-Up of an Initial Series of 101 Patients

Prosthetic repair of coarctation of the aorta with particular reference to Dacron onlay patch grafts and late aneurysm formation