Inferior ST segment changes during acute anterior myocardial infarction: A marker of the presence or absence of concomitant inferior wall ischemia

The significance of inferior ST segment changes during acute anterior myocardial infarction was studied in 60 patients with acute anterior infarction who had angiographic visualization of the entire distribution of the left anterior descending artery after thrombolytic therapy with streptokinase. In 34 patients (Group 1) this artery supplied the anterior wall of the left ventricle up to or including the apex but did not reach the inferior wall; in 16 patients (Group 2) it continued beyond the apex onto the inferior wall of the left ventricle; and in 10 patients with prior inferior infarction (Group 3) it partially supplied the inferior wall of the left ventricle through collateral channels to an occluded right or dominant circumflex coronary artery.Consistent with this anatomy, evidence of inferior wall ischemia was significantly more frequent in Groups 2 and 3 than in Group 1 by thallium-201 scintigraphy (91 versus 7%) and by contrast left ventriculography (91 versus 13%). There was no difference in the magnitude of precordial ST segment elevation among the three groups but the inferior ST segment depression was significantly smaller in Groups 2 and 3 with concomitant inferior wall ischemia than in Group 1 (aVF: −0.5 ± 0.7; −0.5 ± 1.0; −1.8 ± 0.8 mm, respectively; p < 0.001) with 10 of the 26 patients in Groups 2 and 3 having an elevated or isoelectric ST segment in aVF compared with none of the 34 patients in Group 1 (p < 0.001). In patients with inferior ST segment depression, a ratio of ST depression in lead aVF to ST elevation in lead V2 that was less negative than −0.2 was a reliable marker of concomitant inferior wall ischemia.The data suggest that the electrocardiogram can identify patients with anterior infarction who have concomitant inferior wall ischemia due to occlusion of a left anterior descending artery that either also supplies the inferior wall or is the source of collateral flow to a previously occluded posterior descending artery in patients with prior inferior infarction

External counterpulsation therapy improves endothelial function in patients with refractory angina pectoris

AbstractObjectivesThe goal of this study was to investigate the influence of short-term external counterpulsation (ECP) therapy on flow-mediated dilation (FMD) in patients with coronary artery disease (CAD).BackgroundIn patients with CAD, the vascular endothelium is usually impaired and modification or reversal of endothelial dysfunction may significantly enhance treatment. Although ECP therapy reduces angina and improves exercise tolerance in patients with CAD, its short-term effects on FMD in patients with refractory angina pectoris have not yet been described.MethodsWe prospectively assessed endothelial function in 20 consecutive CAD patients (15 males), mean age 68 ± 11 years, with refractory angina pectoris (Canadian Cardiovascular Society [CCS] angina class III to IV), unsuitable for coronary revascularization, before and after ECP, and compared them with 20 age- and gender-matched controls. Endothelium-dependent brachial artery FMD and endothelium-independent nitroglycerin (NTG)-mediated vasodilation were assessed before and after ECP therapy, using high-resolution ultrasound.ResultsExternal counterpulsation therapy resulted in significant improvement in post-intervention FMD (8.2 ± 2.1%, p = 0.01), compared with controls (3.1 ± 2.2%, p = 0.78). There was no significant effect of treatment on NTG-induced vasodilation between ECP and controls (10.7 ± 2.8% vs. 10.2 ± 2.4%, p = 0.85). External counterpulsation significantly improved anginal symptoms assessed by reduction in mean sublingual daily nitrate consumption, compared with controls (4.2 ± 2.7 nitrate tablets vs. 0.4 ± 0.5 nitrate tablets, p <0.001 and 4.5 ± 2.3 nitrate tablets vs. 4.4 ± 2.6 nitrate tablets, p = 0.87, respectively) and in mean CCS angina class compared with controls (3.5 ± 0.5 vs. 1.9 ± 0.3, p <0.0001 and 3.3 ± 0.6 vs. 3.5 ± 0.5, p = 0.89, respectively).ConclusionsExternal counterpulsation significantly improved vascular endothelial function in CAD patients with refractory angina pectoris, thereby suggesting that improved anginal symptoms may be the result of such a mechanism

The distinction between coronary and myocardial reperfusion after thrombolytic therapy by clinical markers of reperfusion

AbstractObjectives. We sought to examine the hypothesis that rapid resolution of ST-segment elevation in acute myocardial infarction (AMI) patients with early peak creatine kinase (CK) after thrombolytic therapy differentiates among patients with early recanalization between those with and those without adequate tissue (myocardial) reperfusion.Background. Early recanalization of the epicardial infarct-related artery (IRA) during AMI does not ensure adequate reperfusion on the myocardial level. While early peak CK after thrombolysis results from early and abrupt restoration of the coronary flow to the infarcted area, rapid ST-segment resolution, which is another clinical marker of successful reperfusion, reflects changes of the myocardial tissue itself.Methods. We compared the clinical and the angiographic results of 162 AMI patients with early peak CK (≤12 h) after thrombolytic therapy with (group A) and without (group B) concomitant rapid resolution of ST-segment elevation.Results. Patients in groups A and B had similar patency rates of the IRA on angiography (anterior infarction: 93% vs. 93%; inferior infarction: 89% vs. 77%). Nevertheless, group A versus B patients had lower peak CK (anterior infarction: 1,083 ± 585 IU/ml vs. 1,950 ± 1,216, p < 0.01; and inferior infarction: 940 ± 750 IU/ml vs. 1,350 ± 820, p = 0.18) and better left ventricular ejection fraction (anterior infarction: 49 ± 8, vs. 44 ± 8, p < 0.01; inferior infarction: 56 ± 12 vs. 51 ± 10, p = 0.1). In a 2-year follow-up, group A as compared with group B patients had a lower rate of congestive heart failure (1% vs. 13%, p < 0.01) and mortality (2% vs. 13%, p < 0.01).Conclusions. Among patients in whom reperfusion appears to have taken place using an early peak CK as a marker, the coexistence of rapid resolution of ST-segment elevation further differentiates among patients with an opened culprit artery between the ones with and without adequate myocardial reperfusion

Third universal definition of myocardial infarction

"Myocardial infarction (MI) can be recognised by clinical features, including electrocardiographic (ECG) findings, elevated values of biochemical markers (biomarkers) of myocardial necrosis, and by imaging, or may be defined by pathology. It is a major cause of death and disability worldwide. MI may be the first manifestation of coronary artery disease (CAD) or it may occur, repeatedly, in patients with established disease. Information on MI rates can provide useful information regarding the burden of CAD within and across populations, especially if standardized data are collected in a manner that distinguishes between incident and recurrent events. From the epidemiological point of view, the incidence of MI in a population can be used as a proxy for the prevalence of CAD in that population. The term ‘myocardial infarction’ may have major psychological and legal implications for the individual and society. It is an indicator of one of the leading health problems in the world and it is an outcome measure in clinical trials, observational studies and quality assurance programmes. These studies and programmes require a precise and consistent definition of MI. In the past, a general consensus existed for the clinical syndrome designated as MI. In studies of disease prevalence, the World Health Organization (WHO) defined MI from symptoms, ECG abnormalities and cardiac enzymes. However, the development of ever more sensitive and myocardial tissue-specific cardiac biomarkers and more sensitive imaging techniques now allows for detection of very small amounts of myocardial injury or necrosis. Additionally, the management of patients with MI has significantly improved, resulting in less myocardial injury and necrosis, in spite of a similar clinical presentation. Moreover, it appears necessary to distinguish the various conditions which may cause MI, such as ‘spontaneous’ and ‘procedure-related’ MI. Accordingly, physicians, other healthcare providers and patients require an up-to-date definition of MI.

Third universal definition of myocardial infarction

"Myocardial infarction (MI) can be recognised by clinical features, including electrocardiographic (ECG) findings, elevated values of biochemical markers (biomarkers) of myocardial necrosis, and by imaging, or may be defined by pathology. It is a major cause of death and disability worldwide. MI may be the first manifestation of coronary artery disease (CAD) or it may occur, repeatedly, in patients with established disease. Information on MI rates can provide useful information regarding the burden of CAD within and across populations, especially if standardized data are collected in a manner that distinguishes between incident and recurrent events. From the epidemiological point of view, the incidence of MI in a population can be used as a proxy for the prevalence of CAD in that population. The term ‘myocardial infarction’ may have major psychological and legal implications for the individual and society. It is an indicator of one of the leading health problems in the world and it is an outcome measure in clinical trials, observational studies and quality assurance programmes. These studies and programmes require a precise and consistent definition of MI. In the past, a general consensus existed for the clinical syndrome designated as MI. In studies of disease prevalence, the World Health Organization (WHO) defined MI from symptoms, ECG abnormalities and cardiac enzymes. However, the development of ever more sensitive and myocardial tissue-specific cardiac biomarkers and more sensitive imaging techniques now allows for detection of very small amounts of myocardial injury or necrosis. Additionally, the management of patients with MI has significantly improved, resulting in less myocardial injury and necrosis, in spite of a similar clinical presentation. Moreover, it appears necessary to distinguish the various conditions which may cause MI, such as ‘spontaneous’ and ‘procedure-related’ MI. Accordingly, physicians, other healthcare providers and patients require an up-to-date definition of MI.