Successful surgical repair of left ventricular rupture after acute myocardial infarction

A 61-year-old man with impending myocardial infarction was admitted and treated by percutaneous transluminal coronary recanalization (PTCR) therapy using Urokinase. Patient's symptoms subsided and his general condition maintained stable until the fifth hospital day, when he developed the signs of cardiac rupture. He was operated upon immediately, and the left ventricular rupture was confirmed and repaired successfully. Patient recovered from the surgery well. This report describes the rare successful surgical case of cardiac rupture secondary to acute myocardial infarction in Japan.     

Revascularization after acute myocardial infarction

Objective: To investigate the influence of hospital teaching status and service availability on rates of revascularization following myocardial infarction. Design: Retrospective cohort study based on province-wide hospital discharge abstracts. Setting: All acute care hospitals in Ontario, Canada’s most populous province (9.7 million). Patients: Patients admitted to hospital between April 1, 1991, and September 30, 1991, with a principal diagnosis of acute myocardial infarction. Measurements: The odds of a patient’s having been referred for revascularization (angioplasty or bypass surgery) within six months of a myocardial infarction were calculated based on the type of hospital to which he or she had initially presented, defined as “teaching” or “nonteaching” or as having or not having interventional facilities onsite (cardiac catheterization and/or revascularization). Odds ratios were adjusted for potential confounding variables, and for possible joint effects of teaching status and on-site interventional capabilities. Results: The patients were more likely to have had revascularization (OR 1.79 95% CI 1.47–2.14, p=0.0001) when they had been admitted to a teaching hospital, and independently were more likely to have been referred for revascularization (OR 1.34; 95% CI 1.09–1.66, p=0.0067) when they had been admitted to a hospital with on-site interventional facilities. There was no interaction between teaching status and service availability regarding referral for revascularization. Conclusion: Teaching status is an important determinant of revascularization following acute myocardial infarction and is independent of service availability, which also influences revascularization rates.     

Transient myocardial ischaemia after acute myocardial infarction

The prevalence and characteristics of transient myocardial ischaemia were studied in 203 patients with recent acute myocardial infarction by both early (6.4 days) and late (38 days) ambulatory monitoring of the ST segment. Transient ST segment depression was much commoner during late (32% patients) than early (14%) monitoring. Most transient ischaemia (greater than 85% episodes) was silent and 80% of patients had only silent episodes. During late monitoring painful ST depression was accompanied by greater ST depression and tended to occur at a higher heart rate. Late transient ischaemia showed a diurnal distribution, occurred at a higher initial heart rate, and was more often accompanied by a further increase in heart rate than early ischaemia. Thus in the first 2 months after myocardial infarction transient ischaemia became increasingly common and more closely associated with increased myocardial oxygen demand. Because transient ischaemic episodes during early and late ambulatory monitoring have dissimilar characteristics they may also have different pathophysiologies and prognostic implications.     

Serum aminoterminal type III procollagen peptide reflects repair after acute myocardial infarction

In 16 patients with acute myocardial infarction and in 15 controls, procollagen type III aminoterminal peptide in serum (PIIINP) was measured consecutively. Serum PIIINP was increased on the second to third postinfarction day (p less than 0.01) and remained elevated for more than 4 months. Peak values were observed on the third to seventh postinfarction day. The individual peak changes were correlated to infarction size calculated from serum CK-MB and serum lactate dehydrogenase (p = 0.60, p = 0.02). The changes in distribution of PIIINP-related antigens in serum after gel chromatography were similar to changes observed during wound healing in humans. PIIINP is cleaved off procollagen type III during the biosynthesis of type III collagen, which characterizes the early stages of repair and inflammation. Our findings suggest that serum PIIINP reflects the repair processes and scar formation following acute myocardial infarction. The serum PIIINP alterations in acute myocardial infarction differ essentially from the changes in myocardial enzymes reflecting myocardial injury. Serum PIIINP may therefore provide new and clinically relevant information on the healing of myocardial infarction.     

Cardiogenic shock after acute myocardial infarction

Cardiogenic shock remains the major cause of death among patients with acute myocardial infarction. Besides supportive therapy there is clear evidence that revascularization of the infarct related artery should be performed as soon as possible with percutaneous transluminal coronary angioplasty. Placement of coronary stents and administration of platelet glycoprotein IIb/IIIa antagonists may further improve outcome. Intra-aortic balloon pumping should be integral part of this treatment strategy but is unfortunately underused in clinical practice. Routine bypass surgery for cardiogenic shock patients is deferred and restricted to selected patients.     

Risk stratification after acute myocardial infarction

In recent years, the characteristics of patients who suffer acute myocardial infarction without complications during hospitalization have changed. In addition, the range of non-invasive studies available for evaluating left ventricular systolic function, residual myocardial ischemia, and myocardial viability in these patients has improved. Left ventricular systolic function and residual ischemia should be evaluated in all patients before release. The non-invasive technique used (exercise test, echocardiography, nuclear cardiology, magnetic resonance imaging) depends on availability, experience, and results at each institution. Coronary arteriography should be performed in patients with significant ischemia or severe left ventricular systolic dysfunction in non-invasive studies. In these cases coronary angiography must be performed to determine if coronary arteries are suitable for revascularization before performing a test of myocardial viability.     

Silent myocardial ischemia after acute myocardial infarction.

Silent ischemia after myocardial infarction has definite prognostic significance but should be interpreted within the context of other prognostic indicators. The rationale for therapeutic intervention is based on the prognostic implications of silent ischemia and the potentially deleterious effect of repeated episodes of ischemia on the integrity of the left ventricle. We measured parameters of ischemia in 20 patients who showed asymptomatic ischemic ST-T changes on exercise testing in the early phase after myocardial infarction. After diltiazem administration, a reduction of exercise-induced ST-T depression from 2.3 +/- 0.8 to 0.7 +/- 0.6 mm (p less than 0.01) occurred, and regional wall-motion score at exercise, determined by radionuclide angiography, improved significantly (p less than 0.02). These and other observations warrant further studies in which the duration, severity and frequency of the ischemic episodes should be quantified and correlated with prognosis after myocardial infarction.     

Transient myocardial ischaemia after acute myocardial infarction.

The prevalence and characteristics of transient myocardial ischaemia were studied in 203 patients with recent acute myocardial infarction by both early (6.4 days) and late (38 days) ambulatory monitoring of the ST segment. Transient ST segment depression was much commoner during late (32% patients) than early (14%) monitoring. Most transient ischaemia (greater than 85% episodes) was silent and 80% of patients had only silent episodes. During late monitoring painful ST depression was accompanied by greater ST depression and tended to occur at a higher heart rate. Late transient ischaemia showed a diurnal distribution, occurred at a higher initial heart rate, and was more often accompanied by a further increase in heart rate than early ischaemia. Thus in the first 2 months after myocardial infarction transient ischaemia became increasingly common and more closely associated with increased myocardial oxygen demand. Because transient ischaemic episodes during early and late ambulatory monitoring have dissimilar characteristics they may also have different pathophysiologies and prognostic implications.     

Cardiac rehabilitation after acute myocardial infarction

At the time of evidence-based medicine, while the proofs of the benefits of cardiac rehabilitation to the coronary multiply, a large number of patients are still managed without any form of rehabilitation. In particular, younger patients with myocardial infarction treated by early reperfusion and older subjects. The objective of in-hospital or ambulatory cardiac rehabilitation is a global coverage of the patient and his/her risk factors, that the short duration of hospitalization in the acute phase does not allow. Several randomized studies, metaanalyses, and registers show a decrease from 20 to 30% of the mortality after cardiac rehabilitation. The benefits of physical training on risk factors modification are demonstrated by numerous works: improvement of lipid parameters and arterial pressure, prevention of diabetes, increased smoking cessation, loss of weight, better overall well-being; besides the management of risk factors, physical training improves exercise capacity, a recognised prognostic factor. The efficiency of cardiac rehabilitation may be comparable with that of the key treatments of coronary artery disease, such as beta-blockers or coronary angioplasty. All these proofs give to the cardiac rehabilitation in post-myocardial infarction a high-level recommendation, grade IA.     

Neuroendocrine activation after acute myocardial infarction

The extent of neuroendocrine activation, its time course, and relation to left ventricular dysfunction and arrhythmias were investigated in 78 consecutive patients with suspected acute myocardial infarction. High concentrations of arginine vasopressin were found within six hours of symptoms, even in the absence of myocardial infarction (n = 18). Plasma catecholamine concentrations also were highest on admission, whereas renin and angiotensin II concentrations rose progressively over the first three days, not only in those with heart failure but also in patients with no clinical complications. Heart failure, ventricular tachycardia, and deaths were associated with extensive myocardial infarction, low left ventricular ejection fraction, and persistently high concentrations of catecholamines, renin, and angiotensin II up to 10 days after admission, whereas in uncomplicated cases concentrations had already returned to normal.     

Anticoagulant therapy after acute myocardial infarction

The use of anticoagulant therapy for patients who have had an acute myocardial infarction is still controversial, mainly because early major studies had conflicting findings, but reanalysis of the data did produce evidence that anticoagulation had clinically and statistically significant benefits. Now more evidence, including the results of a 10-day in-hospital study of low- and high-dose calcium heparin, has been gathered to support using anticoagulants for these patients. The study used the development of left ventricular mural thrombosis, a frequent complication of acute myocardial infarction that carries a high risk for systemic embolic complications, to assess clinical outcome: A reduced incidence of mural thrombosis would be taken to indicate reduced chances that patients would have major systemic emboli. Two-dimensional echocardiography was used to detect thrombi. In the study, the incidence of left ventricular mural thrombosis was significantly lower in the high--than in the low-dose group. Among patients in the high-dose group in whom a mural thrombosis did develop, plasma heparin concentrations were significantly lower and activated partial thromboplastin times were shorter. These data suggest that monitoring plasma heparin levels and anticoagulant response can ensure maximal treatment effectiveness. No significant differences in other outcomes--such as bleeding complications, nonhemorrhagic strokes and mortality--were found between the high- and low-dose treatment groups.     

Early discharge after acute myocardial infarction

Approximately 50% of patients hospitalized with acute myocardial infarction have an uncomplicated course and an excellent prognosis. To be considered as having an uncomplicated course, patients should not have ventricular tachycardia or fibrillation, second or third degree atrioventricular block, pulmonary edema, cardiogenic shock, infarct extension, persistent hypotension, sinus tachycardia, or sustained supraventricular tachycardia occurring within the first 4 days of hospitalization. Patients with recurrent angina in the postinfarction period may also be at increased risk. Early and rapidly progressive rehabilitation programs permit the safe discharge of patients with an uncomplicated course after 7 days. Functional exercise testing before, or soon after, early discharge may identify high-risk patients and alter their management.     

急性心肌梗塞患者的压力反射敏感性测定

目的探讨急性心肌梗塞（ＡＭＩ）后压力反射敏感性（ＢＲＳ）的临床意义。方法分析３１例ＡＭＩ患者和１７例正常对照组的ＢＲＳ、心率变异以及临床情况。结果ＡＭＩ患者３周ＢＲＳ明显小于１７例正常对照组（１０．７±７．２ｍｓ／ｍｍＨｇｖｓ．４．２±１．５ｍｓ／ｍｍＨｇ，Ｐ＜０．０５）；心肌梗塞患者随访中猝死２例，其ＢＲＳ降低最明显；心梗患者的ＢＲＳ与心率变异各项指标无相关性，与年龄、性别、超声射血分数、心肌酶谱等也无相关性；ＢＲＳ有较大个体差异。结论ＢＲＳ在心肌梗塞患者明显下降，并可作为患者的一项独立的预后指标；ＢＲＳ与心率变异是反映患者自主神经的二个不同方面。