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Cardiovascular disease is common in chronic obstructive pulmonary disease (COPD) and raised troponin is common in exacerbations. However, the prevalence of myocardial infarction following hospitalisation for exacerbation of COPD is unknown.Patients aged o40 yrs hospitalised with acute exacerbation of COPD (n5242) with o10 packyrs of cigarette smoking were included in a prospective case series conducted in four hospitals. Patients whose primary presenting complaint was chest pain or who had an alternative diagnosis were excluded. Chest pain histories, serial ECGs and troponin levels were obtained.The mean¡SD age was 69¡9 yrs; 108 (45%) patients were male and almost half were current smokers. 124 (51%; 95% CI 48-58%) patients had chest pain, which was exertional in 62 (26%). 24 (10%) had raised troponin, among whom, 20 (8.3%; 95% CI 5.1-12.5%) had chest pain and/or serial ECG changes, fulfilling the 2007 Universal Definition of Myocardial Infarction. Neither chest pain (p50.77) nor serial ECG changes (p50.39) were associated with raised troponin.Raised troponin, chest pain and serial ECG changes are common in patients admitted to hospital with exacerbation of COPD. Overall, one in 12 patients met the criteria for myocardial infarction. Whether these patients would benefit from further cardiac investigation is unknown.KEYWORDS: Chest pain, chronic obstructive pulmonary disease, ECG, myocardial infarction, troponin C oronary heart disease is a major cause of mortality in chronic obstructive pulmonary disease (COPD) [1,2]. Both conditions share common risk factors, such as smoking and socioeconomic status, and reduced forced expiratory volume in 1 s (FEV1), a characteristic feature of COPD, is an independent risk factor for cardiovascular mortality [3].In studies using routine clinical data, diagnosis with myocardial infarction (MI) appears to be more common following exacerbations in patients with COPD [4,5], while raised troponin has been found to be associated with increased mortality in exacerbation of COPD [6][7][8],Coronary events may present without chest pain [9], can be missed even in simple chest pain presentations [10] and may be more likely to be missed in patients presenting with acute exacerbation of COPD who also report acute breathlessness and chest tightness.Raised troponin is common in patients admitted to hospital with exacerbation of COPD [6][7][8]; however, we are unaware of any prospective study that has investigated this group for clinical or electrocardiography features of MI.Therefore, we undertook a prospective case series to identify the prevalence of MI in patients admitted to hospital with acute exacerbation of COPD. The prevalence of MI was calculated along with 95% confidence intervals using the exact binomial test. In exploratory analyses, associations between patient characteristics and raised troponin concentrations were examined using Fisher's exact test, for which we report all associations where the p-value was ,0.10. Analyses were performed using SAS version 9.2 (SAS In...

Vasodilator therapy has been shown to improve ventricular function in patients with left ventricular failure complicating acute myocardial infarction. Sublingual nitroglycerin also improves ventricular function in these patients but its effects are transient and variable. Infusion of intravenous nitroglycerin in 12 patients with acute infarction resulted in a decrease in left ventricular filling pressure from a mean of 22 plus or minus 2 mm Hg to 12 plus or minus 1 mm Hg (P less than 0.001) associated with a 7 mm Hg decrease in mean arterial pressure (P less than 0.05). Since stroke work index did not change significantly, this represents and improvement in ventricular performance and/or an alteration in ventricular compliance. All six patients in whom serial precordial mapping studies were performed showed a decrease in sigma ST (P less than 0.001). These findings suggest that intravenous nitroglycerin improved left ventricular function and decreased the extent of myocardial ischemia. Longer infusion may act to preserve borderline ischemic myocardium and thus limit infarct size.

Fifty-two patients who survived several arrhythmic cardiac arrests had implantation of an automatic defibrillator along with additional cardiovascular surgery as indicated. The mean follow-up was 14.4 months and the longest was 3 years. In the hospital, the implanted devices identified and reverted 82 episodes of spontaneous and 81 of 99 episodes of induced malignant tachyarrhythmias. There were 62 automatic resuscitations in 17 patients outside the hospital. Twelve patients died; four of the deaths were not witnessed. These deaths represent a 22.9% total and 8.5% sudden-death 1-year mortality rate. Because the expected 1-year mortality in patients without the automatic defibrillator was calculated to be 48%, there was an estimated 52% decrease in anticipated total deaths. The automatic implantable defibrillator can identify and correct potentially lethal ventricular tachyarrhythmias, leading to a substantial increase in 1-year survival in properly selected high-risk patients.

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To evaluate the importance of hepatic blood flow in lidocaine kinetics, we compared indocyanine green clearance, an estimate of hepatic plasma flow, to lidocaine clearance in 26 patients, half with and half without congestive heart failure, who received a lidocaine infusion for 24 hours as clinically indicated. The results demonstrated that patients with congestive heart failure had significantly higher steady-state lidocaine levels (6.8 +/- 3.6(S.D.) vs. 2.9 +/- 0.9 microgram per milliliter, P less than 0.005) and reduced lidocaine clearance (3.8 +/- 1.4 vs. 10.9 +/- 3.1 ml per minute per kilogram, P less than 0.005) than patients without heart failure. Potentially subtherapeutic or toxic lidocaine levels were found in 10 patients. The regression line (y = 0.3 + 1.07 x) relating clearance of lidocaine to that of indocyanine green was linear (r = 0.95, P less than 0.001). Since indocyanine green clearance can be determined rapidly and noninvasively, it offers the potential of predicting lidocaine dosage requirements with avoidance of toxicity or suboptimum therapy.

SUMMARY This study was performed to determine whether nitroglycerin (NG) can increase collateral flow to ischemic myocardium and reduce ultimate infarct size. Permanent occlusion of the mid-circumflex coronary artery was produced in 43 previously instrumented conscious dogs and within 3 minutes, 6-hour intravenous infusions were begun of saline (controls, n = 18), NG in doses to reduce mean arterial pressure by 10% but not below 90 mm Hg (n = 15), or NG followed by methoxamine (MX) to correct the NG-induced fall in blood pressure (n = 10). After sacrifice 2 days later, the occluded coronary bed was defined by postmortem coronary arteriography and masses of infarct and occluded bed were measured by planimetry of weighed rings of the left ventricle (LV). Infarct size was significantly less with NG than saline, both as a percent of LV (12.1 vs 6.4%, p < 0.05) and as a percent of occluded bed (32.0 vs 15.9%,p < 0.005). NG plus MX did not reduce infarct size more than NG alone: 6.6 vs 6.4% of LV, and 16.0 vs 15.9% of occluded bed. Masses of LV and occluded bed did not differ significantly among the three groups. Coronary blood flow (CBF), measured by 7-10-,gm radioactive microspheres, increased by more than 50% throughout the occluded bed (p < 0.005) after NG, and was more than the spontaneous increase seen in controls (p < 0.05), but MX had no additional effect on CBF over NG alone. Six-hour infusions of NG therefore decreased infarct size and improved CBF, and addition of MX to reverse the systemic effects of NG did not lessen the benefit. The results suggest that under the conditions of this study, myocardial protection by NG did not depend on a decrease in myocardial oxygen demands, but rather on an increase in collateral flow resulting from a direct vasodilating action of NG on the coronary bed.INTRAVENOUS NITROGLYCERIN (NG) has been shown to reduce ST-segment elevation in dogs'`4 and man5-9 in the early stages of myocardial infarction, and to decrease myocardial necrosis after 5-hour coronary occlusions in dogs.2 NG dilates systemic and coronary vessels, so the beneficial effects in acute myocardial infarction may be caused by a net reduction of myocardial oxygen demands associated with decreases in afterload and preload, or to increases in collateral flow to ischemic myocardium,'0'9 or both. As perfusion pressure is a major factor in limiting infarct size' and determining collateral flow,20 correction of NG-induced hypotension and reflex tachycardia with concomitant a-adrenergic agonists has been used and found to result in less ST-segment elevation,"'1, 17 more collateral flow,'6 18 and less necrosis2 in dogs. Bache'8 found that NG alone increased flow to transiently ischemic myocardium in conscious dogs, while the combination of NG and phenylephrine-induced hypertension produced even greater increases. These studies" 2,16.18 whether NG alone given after permanent coronary occlusion can significantly increase collateral flow and decrease ultimate infarct size.We studied the effects of NG on collateral flow ...

The purpose of the present study was to examine at autopsy the effect of multiple defibrillations on the myocardium and the pathologic consequences of short- and long-term placement of the intravascular and interpericardial leads of the automatic implantable cardioverter-defibrillator. Twenty-five patients were examined at autopsy; 8 of them underwent lead implantation only and 17 received both leads and the automatic implantable cardioverter-defibrillator. Twelve patients (48%) died of ventricular tachycardia or ventricular fibrillation; seven (28%) died of other causes. Acute pericarditis occurred in all patients, resulting in a localized, progressive fibrosis around the apical patch lead without giving rise to pericardial restriction. Thrombus formation was associated with the superior vena cava spring electrode in four patients (17%) and the right ventricular rate-sensing electrode in one patient (4%). Asymptomatic pulmonary emboli occurred in two patients (8%). In one patient who underwent defibrillation 59 times, superior vena cava changes consisted of vein wall destruction, fibrosis and thrombus formation. Pathologic changes under the apical patch related to defibrillation were observed in seven patients; two of these had fewer than 5 defibrillations, one had 8 defibrillations and four had 21 to 74 defibrillations. These changes consisted of contraction band necrosis in four patients, vacuolar cytoplasmic clearing and loss of myocytes confined to the myocardium under the patch electrode in five patients who had multiple defibrillations. The observed pathologic changes were estimated to affect less than 2% of the total myocardial mass. Thus, the automatic implantable cardioverter-defibrillator lead system and multiple defibrillations result in localized myocardial injury confined to the tissue under the patch electrode.(ABSTRACT TRUNCATED AT 250 WORDS)