The role of the coronary collateral circulation in limiting myocardial ischemia and infarct size

The role of coronary collateral circulation in limiting ischemia and infarction has been studied prospectively. Transient occlusion of a coronary artery angioplasty has provided evidence that collateral circulation decreases wall motion abnormalities, ST segment changes, and lactate production. Patients who have collateral flow also have a better outcome after coronary artery dissection and acute closure than patients without collateral flow. Collateral circulation also limits infarct size during acute myocardial infarction with and without thrombolysis. Although collateral flow may decrease coronary artery bypass graft patency in certain subgroups of patients, the perioperative infarct rate and mortality is decreased. Growth factors have been identified that increase the development collateral circulation and may improve ventricular function in the setting of myocardial infarction.     

Anabolic steroid abuse and cardiac death

OBJECTIVE: To examine the relationship between anabolic steroid abuse and cardiac death. We report the first two cases in Australia. They are the only reported cases in which the anabolic steroid oxymesterone has been detected. This compound has never been approved for use in Australia. CLINICAL FEATURES: Two footballers, aged 18 and 24, sustained fatal cardiac arrests while at training sessions. Both were considered fit and healthy. OUTCOME: Autopsy revealed features of a hypertrophic cardiomyopathy in the 18-year-old; the 24-year-old had findings of a myocarditis. In both cases the coronary arteries were normal and there was no evidence of coronary thrombosis. Urine in both subjects contained the anabolic steroid oxymesterone. CONCLUSIONS: There are limited clinical uses for anabolic steroids but they are widely abused by athletes in attempts to alter lean body mass and strength. Acute non-fatal myocardial infarction was first reported in 1988 and fatal myocardial infarction in 1990. While a causal relationship is hard to prove, it is possible that the anabolic steroid contributed to the increase in cardiac size in the first subject and may have increased his responsiveness to catecholamines causing an arrhythmogenic event. In the second, the inflammatory changes could have provided the focus for an arrhythmia. It would appear that anabolic steroid abuse should be considered in any athlete presenting with an acute vascular event.     

Influence of bypass grafting to the infarct artery on late potentials in coronary operations

BACKGROUND: Late potentials (LPs) after myocardial infarction identify the risk of arrhythmic events and sudden death, and the absence of anterograde flow in the infarct-causing occluded coronary artery frequently is associated with LPs on signal-averaged electrocardiography. The present study was designed to clarify the influence of revascularization of the infarct artery on the LPs in the late course after myocardial infarction. METHODS: We studied 21 patients after myocardial infarction with positive LPs who had at least one occluded infarct coronary artery. We investigated the LPs on signal-averaged electrocardiograms on the day of elective coronary artery bypass grafting (CABG) and 1 week after CABG. RESULTS: There were 25 infarct arteries in the study patients, 13 of which were grafted. The positive LPs disappeared soon after CABG in 13 patients, 10 of whom had grafts to all of the infarct arteries. The LPs persisted in 8, who received no graft to the infarct artery. One week after CABG, the LPs were still present in 4, all of whom had no graft to the infarct right coronary artery. CONCLUSIONS: In patients with positive LPs late after myocardial infarction, grafting to the infarct artery eliminated the LPs soon after CABG.     

Short-term versus long-term use of nitrates in acute myocardial infarction

While previous experimental and small-scaled clinical studies have shown intravenous administration of nitroglycerin in the setting of acute myocardial infarction reduced infarct size and diminished the frequency of mechanical complications, its effect on short-term and long-term outcome has not been established. Recently, two large-scaled clinical trials, GISSI-3 and ISIS-4, have demonstrated unexpected neutral effect of nitrates on subacute phase mortality after myocardial infarction. Long-term nitrate treatment, however, has been indicated by three independent clinical studies that it may increase cardiac events in patients with healed myocardial infarction. Although a large-scaled randomized clinical trial is required to confirm the deleterious effect of nitrates on long-term outcome after myocardial infarction, routine use of nitrates in chronic phase of coronary heart disease cannot be recommended.     

Improved long-term prognosis after myocardial infarction 1984-1991

AIMS: We set out to examine whether long term prognosis in terms of 2-year mortality after myocardial infarction has improved after the introduction of intravenous beta-blockers, nitroglycerin infusion, aspirin and thrombolytics, in an unselected population of patients hospitalized with a myocardial infarction. METHODS AND RESULTS: We investigated retrospectively 3791 acute myocardial infarctions in 3187 G?teborg women and men (1039 women and 2148 men), who were consecutively admitted to the coronary care unit at the Ostra hospital during 1984-1991. Throughout this period, data were entered continuously into the coronary care unit database. Mortality data were collected through the Swedish cause-specific mortality register. The primary end-point was mortality within 2 years after the onset of the index infarction. Two-year mortality decreased from 36% in 1984 to 25% in 1991. In a Cox regression model (including myocardial infarctions up to 1993) year of hospitalization, age, diabetes mellitus, sex, prior myocardial infarction and indeterminable infarct location all had a significant impact on survival after myocardial infarct. Thrombolytic therapy and hypertension had no prognostic significance. CONCLUSION: Against a background of radical changes in the treatment of acute myocardial infarction during 1984-1991 we have seen decreasing in-hospital mortality as well as a substantial decrease in 2-year mortality.     

Sudden disappearance of electrocardiographic pattern of anteroseptal myocardial infarction. Result of superimposed acute posterior myocardial infarction

In a 76-year-old man an electrocardiographic pattern of acute anteroseptal myocardial infarction disappeared suudenly. At necropsy, a more recent posterior myocardial infarct was found, in addition to an acute anteroseptal infarct. "Normalization" of the electrocardiogram from the pattern of anteroseptal myocardial infarction in this case resulted from the loss of opposing electromotive forces in the posterior wall because of posterior infarction.     

Myocardial infarction complicated by ventricular septal rupture in a patient with polycythemia vera and minimal coronary ectasia

Although it is known that patients with polycythemia vera (PV) are at increased risk of myocardial infarction (MI) secondary to thrombosis, ventricular septal rupture in this setting has never been reported. Ventricular septal rupture complicating a small anteroseptal MI is reported in a patient with PV and with only minimal ectasia of the left anterior descending coronary artery. Despite small infarct size these patients may be predisposed to myocardial hemorrhage, increasing the likelihood of myocardial rupture.     

Arrhythmias associated with acute myocardial infarction and thrombolysis

Ninety percent of patients with acute myocardial infarction have some cardiac rhythm abnormality, and approximately twenty-five percent have cardiac conduction disturbance within 24 hours following infarct onset. Almost any rhythm disturbance can be associated with acute myocardial infarction, including bradyarrhythmias, supraventricular tachyarrhythmias, ventricular arrhythmias, and atrioventricular block. With the advent of thrombolytic therapy, it was found that some rhythm disturbances in patients with acute myocardial infarction may be related to successful coronary artery reperfusion. This article addresses the role and treatment of arrhythmias and conduction disturbances that complicate the course of patients with acute infarction and thrombolysis.     

Acute myocardial infarction: early recognition and management from the home healthcare nurses perspective

Acute myocardial infarction is the number one killer of men and women in the United States. Early recognition and treatment has been shown to decrease mortality and infarct size, and to improve left ventricular function. The home healthcare nurse is in a key position to perform a swift, pertinent assessment that can detect an acute myocardial infarction, provide the patient with the valuable information to decrease the time delay until thrombolytic therapy is initiated, participate in the rehabilitation post-myocardial infarction, and provide education and counseling for coronary heart disease risk reduction.     

Subendocardial myocardial ischemia as assessed with myocardial contrast echocardiography in patients with ischemic heart diseases

Myocardial contrast echocardiography was used to characterize changes in the regional and transmural myocardial blood flow distribution that were provoked by rapid atrial pacing stress in patients with coronary artery diseases. In patients with coronary organic stenosis, a decrease in the myocardial contrast-enhancement in the subendocardial half after rapid atrial pacing was associated with stress-induced chest pain and electrocardiographic ST-T changes. The decrease in the myocardial contrast-enhancement in the subendocardial half after rapid atrial pacing was not observed in patients without coronary stenosis or after coronary angioplasty. Thus, the finding was considered to reflect myocardial ischemia. Pacing-induced decreases in myocardial contrast-enhancement were observed in some patients with old myocardial infarction and significant resting coronary collaterals. In these patients, myocardial ischemia was considered to have developed at rapid pacing because collateral function was good enough to perfuse the infarct myocardium at rest, but was not good enough to prevent myocardial ischemia at stress. Thus, myocardial contrast echocardiography seems to be particularly useful in assessing myocardial ischemia at stress due to coronary stenosis in patients with angina pectoris and due to poor dynamic collateral function in patients with old myocardial infarction.     

The effects of thermogenic agents on hindlimb oxygen consumption in the dog: ICI D7114 and noradrenaline

OBJECTIVES: The purpose of this study was to test the hypothesis that the diameter of the recipient coronary artery of the well developed collateral circulation in patients with acute myocardial infarction increases because of the augmented intravascular pressure caused by subsequent collateral development. BACKGROUND: It is well known that collateral circulation develops after acute myocardial infarction. However, some patients have a well developed collateral circulation at the onset of infarction, which may limit the angiographic evaluation of further development of collateral circulation. METHODS: We measured the diameter of the donor and recipient arteries of the collateral circulation by means of a computer-assisted analysis system in seven patients with acute myocardial infarction who had a totally occluded infarct-related coronary artery during the acute and chronic stages of infarction. All coronary angiograms were obtained after the administration of sublingual nitroglycerin. The measurement was repeated immediately after (within 6 h) and late after (42 +/- 11 days) the onset of acute myocardial infarction. RESULTS: The diameter of the donor artery remained unchanged (1.32 +/- 0.98 vs. 1.42 +/- 1.12 mm). In contrast, the diameter of the recipient artery increased from 1.25 +/- 0.63 to 1.55 +/- 0.61 mm (p < 0.01). These changes in coronary artery diameter were associated with an improvement in regional myocardial wall motion at rest in infarct areas (6.7 +/- 7.0% vs. 13.6 +/- 10.7%, p < 0.05). CONCLUSIONS: These findings indicate that serial measurement of coronary artery diameter is useful for the evaluation of collateral development after acute myocardial infarction.     

Clinical and angiographic features of patients with an occluded versus a patent infarct vessel after intravenous streptokinase for acute myocardial infarction

Despite early treatment with thrombolytic agents for acute myocardial infarction, a significant portion of patients fail to achieve a patent infarct artery. To study the various factors related to achieving patency in the infarct vessel, 201 patients who received streptokinase within six hours of symptoms were studied. All patients underwent cardiac catheterization during the same hospitalization at 5.40 +/- 3.26 days after admission. Forty-five (22.4%) patients were found to have an occluded infarct artery (group 1) and 156 (77.6%) had a patent infarct vessel (group 2). There was no difference in the time from onset of symptoms to receiving streptokinase between the two groups. The two groups were similar to each other with regard to age, gender, history of myocardial infarction or angina, and major risk factors for coronary disease. Coagulation parameters before and after streptokinase therapy, reflecting the lytic state, were similar in both groups. The left ventricular end diastolic pressure was significantly higher and the left ventricular ejection fraction was significantly lower in group 1 than in group 2. These observations suggest that despite early initiation of thrombolytic therapy in patients with acute myocardial infarction, a significant portion of patients fail to achieve a patent infarct artery. This failure cannot be explained by the observed clinical parameters or the lytic state after streptokinase.     

Early angiotensin converting enzyme inhibitor therapy after experimental myocardial infarction prevents left ventricular dilation by reducing infarct expansion: a possible mechanism of clinical benefits

OBJECTIVE: To examine the effects of early angiotensin-converting enzyme (ACE) inhibitor therapy after myocardial infarction on infarct expansion in an experimental rat model. BACKGROUND: ACE inhibitor therapy within 24 h of acute myocardial infarction (AMI) reduces mortality by unknown mechanism(s). METHODS: Rats underwent permanent coronary artery occlusion. A treated group received enalapril (1.9+/-0.2 mg/kg) daily in drinking water beginning 2 h after coronary artery occlusion, a time too late to reduce infarct size. Rats were sacrificed 2 days or 2 weeks after myocardial infarction. Hearts were arrested and fixed at a constant pressure, then sectioned and photographed for morphometric analysis. RESULTS: Infarcts in the control group expanded between 2 days and 2 weeks after myocardial infarction (expansion index 0.7+/-0.1 versus 2.5+/-0.4, P< 0.05). However, infarct expansion remained unchanged in the enalapril group between 2 days and 2 weeks after myocardial infarction (expansion index 0.8+/-0.1 versus 1.3+/-0.1, NS). Two weeks after myocardial infarction, the enalapril group had fewer expanded infarcts than the control group (expansion index 1.3+/-0.1 versus 2.5+/-0.4, P< 0.05). While left ventricular volume increased in the control group between 2 days and 2 weeks after myocardial infarction (0.17+/-0.01 ml versus 0.36+/-0.03 ml, P< 0.05), it remained constant in the enalapril group (0.22+/-0.02 ml versus 0.25+/-0.03 ml, NS). Two weeks after myocardial infarction, the left ventricles were larger in the control group than in the enalapril group (0.36+/-0.03 ml versus 0.25+/-0.03 ml, P< 0.05). CONCLUSIONS: Treatment with enalapril initiated 2 h after AMI prevented left ventricular dilation by limiting infarct expansion. This may explain the mechanism by which ACE inhibitor therapy started within 24 h of an AMI improves survival 5-6 weeks after infarction.     

Aneurysm of the right colic artery

Primary PTCA as a means of reestablishing coronary blood flow in the infarct related artery is preferable in certain subgroups of patients with acute myocardial infarction. While the success rate of primary PTCA is very high, the procedure is not without risk. We report a case of hemodynamic collapse during PTCA due to an Amplatz guide catheter-induced, acute, and reversible aortic insufficiency. With the increasing use of the left Amplatz catheter for better guide support during PTCA, this unusual and previously unreported complication should be borne in mind.     

Direct percutaneous transluminal coronary angioplasty in acute myocardial infarction. Predictors of short-term outcome and the impact of coronary stenting. Study Group of The Arbeitsgemeinschaft Leitender Kardiologischer Krankenhaus?rzte (ALKK)

BACKGROUND: Direct percutaneous transluminal coronary angioplasty (PTCA) is widely accepted in the treatment of acute myocardial infarction since excellent results had been reported from several small randomized trials. Less favourable results were observed in large-scale registries. In particular, the use of stents in acute myocardial infarction has become common practice without documented evidence of clinical efficacy. METHODS: Data were analysed from a registry of all consecutive percutaneous transluminal coronary angioplasty procedures from 62 centres in Germany, including 2331 direct percutaneous transluminal coronary angioplasty in acute myocardial infarction from July 1994 to April 1997. RESULTS: The overall angiographic success rate of percutaneous transluminal coronary angioplasty, defined as complete antegrade perfusion of the infarct vessel, was 87%. In-hospital mortality was 11.2%. The most important predictor of death was the presence of cardiogenic shock in 15% of patients, of whom 52% died. Mortality in patients without shock was 3.9%. Failed percutaneous transluminal coronary angioplasty was associated with a mortality of 36%. Further independent predictors of death were older age, multivessel disease, and anterior myocardial infarction. Stents were used in 4.1% of the procedures in 1994, increasing to 53% in 1997. However, this was not accompanied by improved clinical outcome. Mortality with coronary stenting was 9.9% vs 11.6% without stents (ns). CONCLUSIONS: Direct percutaneous transluminal coronary angioplasty is a valuable treatment strategy in acute myocardial infarction, although the results are less exceptional than reported from some highly specialized centres. Failed percutaneous transluminal coronary angioplasty seems to be harmful, thus outweighing much of the benefit from successful procedures. Stents did not improve the clinical outcome significantly, despite technically successful placement in 98%. Mortality from cardiogenic shock continues to be excessively high despite direct PTCA.     

Two cases of acute myocardial infarction associated with aplastic anemia during treatment with anabolic steroids

Thrombosis is a rare complication in patients with aplastic anemia because of the presence of coincidental thrombocytopenia. We have recently treated two cases, a 61-year-old male and a 59-year-old female, with acute myocardial infarction associated with aplastic anemia. Although their platelet counts were lower than normal in spite of treatment with anabolic steroids for aplastic anemia, the coronary angiographic findings strongly suggested coronary thrombosis in both cases. Anabolic steroids, which have been commonly used for the treatment of aplastic anemia, are a possible risk factor for coronary thrombosis because they have an accelerating effect on thrombus formation. We report two very rare but clinically important cases.     

Magnitude and time course of microvascular obstruction and tissue injury after acute myocardial infarction

BACKGROUND: Microvascular obstruction within an area of myocardial infarction indicates worse functional recovery and a higher risk of postinfarction complications. After prolonged coronary occlusion, contrast-enhanced MRI identifies myocardial infarction as a hyperenhanced region containing a hypoenhanced core. Because the time course of microvascular obstruction after infarction/reperfusion is unknown, we examined whether microvascular obstruction reaches its full extent shortly after reperfusion or shows significant progression over the following 2 days. METHODS AND RESULTS: Seven dogs underwent 90-minute balloon occlusion of the left anterior descending coronary artery (LAD) followed by reflow. Gadolinium-DTPA-enhanced MRI performed at 2, 6, and 48 hours after reperfusion was compared with radioactive microsphere blood flow (MBF) measurements and myocardial staining to define microvascular obstruction (thioflavin S) and infarct size (triphenyltetrazolium chloride, TTC). The MRI hypoenhanced region increased 3-fold during 48 hours after reperfusion (3.2+/-1.8%, 6.7+/-4.4%, and 9.9+/-3.2% of left ventricular mass at 2, 6, and 48 hours, respectively, P<0.03) and correlated well with microvascular obstruction (MBF <50% of remote region, r=0.99 and thioflavin S, r=0.93). MRI hyperenhancement also increased (21.7+/-4.0%, 24.3+/-4.6%, and 28.8+/-5.1% at 2, 6, and 48 hours, P<0.006) and correlated well with infarct size by TTC (r=0.92). The microvascular obstruction/infarct size ratio increased from 13.0+/-4.8% to 22.6+/-8.9% and to 30.4+/-4.2% over 48 hours (P=0.024). CONCLUSION: The extent of microvascular obstruction and the infarct size increase significantly over the first 48 hours after myocardial infarction. These results are consistent with progressive microvascular and myocardial injury well beyond coronary occlusion and reflow.     

Evolution of the CCU from rhythm, function and protection to reperfusion and beyond: a personal journey and perspective

OBJECTIVE: To trace the evolution of coronary care and the management of acute coronary syndromes. STUDY SELECTION: Landmark articles and selected personal experiences. DATA SYNTHESIS: The evolution of coronary care falls into four major categories and decades: the 1960s during which it was recognized that resuscitation from myocardial infarction through closed chest resuscitation (CPR) and defibrillation were possible and attention was directed towards the recognition and management of cardiac dysrhythmias; in the 1970s it became appreciated that infarct size was directly related to prognosis and modifiable. Hemodynamic monitoring was introduced and made significant contributions to the identification of prognostic subsets and the pharmacologic management of pump failure; thrombolytic therapy was introduced in the 1980s and has markedly altered the care of patients with acute myocardial infarction who have ST elevation. Primary angioplasty is an important therapeutic alternative especially in selected subsets; in the 1990s attention shifted to opportunities for favourable impact on ventricular remodelling after myocardial infarction, more cost effective therapy, enhancement of the process of care, and the identification of low and high risk subsets that might lead to more efficient diagnostic triage early after symptom presentation. CONCLUSIONS: There has been a profound evolution of the coronary care unit since its inception in Canada in 1962. It has proved a remarkable environment for education and clinical investigation through which patient care has been substantially improved. Lessons learned have favourably impacted on the process of care, the creation of new national and international standards and a fertile environment for continuous future evaluation and improvement.     

Molecular basis of fibrinolysis, as relevant for thrombolytic therapy

The fibrinolytic system comprises an inactive proenzyme, plasminogen, that is converted by plasminogen activators to the active enzyme, plasmin, that degrades fibrin. Two physiological plasminogen activators have been identified: tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA). Plasminogen activation for clot lysis is regulated by specific molecular interactions between tissue-type plasminogen activator (t-PA), plasminogen and fibrin, whereby the lysine-binding sites of the plasminogen molecule play a crucial role by mediating its binding to fibrin, and by controlling the inhibition rate of plasmin by alpha 2-antiplasmin. The recognition that thrombosis within the infarct related coronary artery plays a major role in the pathogenesis of acute myocardial infarction and the observation that early administration of thrombolytic agents results in recanalization of occluded coronary arteries, have provided the basis for the development of thrombolytic therapy in acute myocardial infarction. The elucidation of the biochemical mechanism of fibrin-specific plasminogen activation has fueled the hope that specific and efficacious thrombolytic agents might become available. Comparative studies between the non-fibrin-selective streptokinase and fibrin-selective recombinant t-PA (rt-PA) have shown a difference in efficacy for early coronary artery recanalization, whereas the GUSTO trial has established that clinical benefit in patients with acute myocardial infarction is indeed correlated with the rapidity and frequency of sustained recanalization and that effective thrombolysis requires adequate anticoagulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

In vivo antinociceptive activity of anti-rat mGluR1 and mGluR5 antibodies in rats

Conflicting results of an association between the human platelet antigen 1b (HPA-1b or PlA2) allele and the risk of myocardial infarction and coronary artery disease have been reported. To assess the reason for this discrepancy, we determined the HPA-1 genotype in 298 men who had undergone coronary angiography, including 124 individuals with myocardial infarction, 83 individuals with coronary artery disease but no history of myocardial infarction, and 91 control patients. Among patients with acute or recent onset myocardial infarction (< 1 year), the prevalence of HPA-1b was higher than among patients with coronary artery disease but without myocardial infarction (33 percent vs. 14 percent, p = 0.016). In patients under 60 years of age this difference was even more pronounced (45 percent vs. 15 percent, p = 0.003). Unlike conventional risk factors HPA-1b does not represent a risk factor for coronary artery disease itself but appears to be associated with increased platelet thrombogenicity.