The misuse of cardiopulmonary resuscitation

Over a 41-month period, 1,233 "Code Blues" were retrospectively reviewed. Twenty-five codes on infants and children < 16 years of age were eliminated from the study group. The adult survivors of 1,208 codes numbered 243 (20.1%). Clinical chart review revealed that 49 (4.0%) did not involve cardiopulmonary resuscitation (CPR) or intubation and were "non-codes." Of the remaining 1,159 codes, there were 194 (16.7%) survivors. Of these survivors, 102 (52.5%) were patients with respiratory distress or failure and required intubation only. No CPR was needed. Thus, only the remaining 92 survivors of the 1,057 codes were cardiac cases for which CPR was appropriate (8.7% survival). Ventricular tachycardia and fibrillation, promptly defibrillated, was the most important rhythm factor for survival. Underlying ischemic heart disease (acute myocardial infarction and chronic ischemic heart disease with arrhythmia) was the most common underlying disease entity among the survivors. CPR performed in the group of patients unlikely to survive was expensive.     

New strategies for intraoperative myocardial protection

In the past, most strategies for intraoperative myocardial protection were developed in models using nondiseased adult hearts from various animal species. In the clinical setting, however, myocardial status in cardiac patients may be quite different and there is a need to adapt our current protective strategies to the actual pathophysiological status of the heart. In the immature heart as well as in the senescent heart, current protective techniques have been shown to be deficient and further research is required. New insights have been gained into the pathophysiological processes underlying chronic ischemic left ventricular dysfunction in the "hibernating" myocardium. It has been shown that viability in these hearts is associated with subcellular alterations related to dedifferentiation of the myocytes. This finding explains the delayed recovery in function of these hearts after revascularization and the need for intraoperative protective strategies focusing on the prevention of stunning in the nonhibernating segments. Tepid continuous retrograde blood cardioplegia is suggested as the optimal technique. Unraveling the mechanisms of preconditioning in the heart and understanding endogenous myocardial protection may provide clues for novel cardioprotective techniques. Adenosine itself may be used as an adjunct to cardioplegia, and treatment with adenosine regulating agents or nucleoside transport inhibitors shows promising results. Like adenosine, other hyperpolarizing agents (potassium-channel openers) are suggested for arrest of the heart instead of the depolarizing agents commonly used in cardioplegia. Finally, the role of Na(+)-H+ exchange in the development of ischemic and postischemic injury has become more clear. By the use of a new selective Na(+)-H+ exchange inhibitor, postischemic contracture can be dramatically reduced and contractility improved. This opens prospective approaches in emergency coronary bypass surgery for evolving myocardial infarction.     

Influence of age on enzyme activities of pyrimidine metabolism in the chicken heart

We and others found that cardioprotection is acquired not only soon after, but also 24 h after ischemic preconditioning in canine and rabbit myocardial infarction models (second window of protection). However, a second window phenomenon against myocardial infarction was dependent on species limitations and has not been observed in porcine hearts. In this study, we examined whether the "second window of protection" against myocardial infarction is observed in the rat heart. In the ischemic preconditioning (IP) group, the left main coronary artery (LCA) of rats was occluded four times for 3 min. each separated by reperfusion for 10 min. After 0, 3, and 24 h, the rats were subjected to a 20-min LCA occlusion followed by 48-h reperfusion. At 0 and 24 h after IP, infarct size and the incidence of ventricular fibrillation (VF) during ischemia were significantly reduced compared with corresponding sham-operated groups without preconditioning. After 3 h of IP, there were no differences either in the incidence of VF during ischemia or in infarct size. Manganese superoxide dismutase (Mn-SOD) content in ischemic (LCA) region of myocardium significantly increased as compared with that of sham-operated rats 24 h after IP. Treatment with N-2-mercaptopropionyl glycine, an antioxidant and a hydroxyl radical scavenger, during IP abolished the early-phase (0 h after IP) and late-phase (24 h after IP) cardioprotection and the corresponding late increase in Mn-SOD content. These results indicate that a "second window of protection" against myocardial infarction also exists in rat hearts and the induction of an intrinsic scavenger, Mn-SOD, via free radical production during IP may be important in the second window of protection.     

Biochemical markers in acute myocardial infarct

Exact and early diagnosis of acute myocardial infarction is essential for the subsequent routine management of this frequent cardiovascular disease. At present, the clinical biochemistry possesses a set of more or less cardiospecific protein markers for early detection of myocardial ischemic damage. After the admission of patient to the hospital, serial estimations of rather non-specific enzyme activities (creatine kinase, its MB-izoenzyme, lactate dehydrogenase, hydroxybutyrate dehydrogenase) are currently used for the detection of acute myocardial infarction and for the further monitoring of the patient and managing his therapy. In the past decade, many cardiospecific biochemical markers were discovered and gradually introduced into the routine clinical practice. The most perspective markers are some molecules of contractile proteins of heart myofibrils (troponins, myosin chains) as well as "rediscovered" myoglobin. The aim of this review article is to inform about the commonly used, as well as about the new biochemical markers, to discuss some problems of diagnostic strategy in the early and exact detection of ischemic myocardial damage and to attract attention to the difficulties. However its disadvantage resides in its presence in both myocardium and skeletal muscles which arise when the diagnosis of acute myocardial infarction is prematurely excluded from consideration and such patients are discharged too soon from hospital. (Fig. 1, Tab. 1, Ref. 72.)     

Elevation of plasma angiotensinogen in rats with experimentally induced nephrosis

Oxidant injury contributes to myocardial stunning, and cardiac ischemic and reperfusion injury. Vitamin E is the major--and perhaps the only--lipid soluble, chain-breaking antioxidant in the heart. Vitamin E and its analogues potentially offer significant advantages for the prevention of ischemic and reperfusion injury. Recent investigations have suggested that modified vitamin E analogues may be more efficacious than vitamin E and may permit myocardial salvage from acute myocardial ischemic injury.     

Criteria of myocardial ischemia in bicycle ergometry of patients with stenosing arteriosclerosis of the cardiac coronary arteries depending on the initial ECG at rest

The sensitivity of various criteria of the physical exercise test in revealing myocardial ischemia was studied in 2 groups of patients with ischemic heart disease: 1st group of 64 patients with normal ECG at rest, 2nd group of 96 patients with cicatricial changes in the myocardium. Selective coronography demonstrated atherosclerotic narrowing (stenosis of more than 70%) of one or more coronary arteries of the heart in all patients. During physical exercise an attack of angina pectoris without "ischemic" changes on the ECG occurred in 36.1% of patients of the 1st group and in 22.4% of patients of the 2nd group. The frequency of other clinical signs of cessation of the exercise (dyspnoea, change of arterial pressure, extrasystole and others) was three and a half times higher in patients with cicatricial changes in the myocardium. It is concluded that the frequency with which signs of myocardial ischemia are revealed during physical exercise depends not only on the pronounced character of the pathological coronary condition and the development of collateral circulation but also by the sensitivity of the separate ECG leads and the presence and localization of cicatricial changes in the myocardium.     

Effect of MCI-154, a cardiotonic agent, on regional contractile function and myocardial oxygen consumption in the presence and absence of coronary artery stenosis in dogs

The effects of MCI-154 (6-[4-(4'-pyridyl)aminophenyl]-4,5-dihydro-3(2H)- pyridazinone hydrochloride.3H2O), a cardiotonic agent with calcium sensitizing actions, on regional contractile function and myocardial oxygen consumption (MVO2) were studied in the dog hearts with and without partial occlusion of the left anterior descending coronary artery and compared with those of dobutamine. Segment shortening by sonomicrometry, regional myocardial blood flow by microspheres and the oxygen content of coronary venous blood drawn from the ischemic left anterior descending coronary artery area were simultaneously measured. The ischemic zone segment shortening and left ventricular (LV) dP/dtmax were decreased after partial occlusion. The infusion of MCI-154 starting 20 min after ischemia improved the depressed segment shortening and LV dP/dtmax without increasing the ischemic zone MVO2 and regional myocardial blood flow. In the nonischemic hearts, MCI-154 did not increase MVO2 and coronary blood flow despite the augmentation of myocardial contractility. MCI-154 decreased LV end-diastolic pressure and systemic blood pressure. On the other hand, dobutamine failed to increase the ischemic zone segment shortening, but the drug increased MVO2, coronary blood flow and LV dP/dtmax in both ischemic and nonischemic hearts. These results indicate that MCI-154 alleviates the ischemic contractile failure without increasing myocardial oxygen demand. Thus, MCI-154 may be useful in the management of heart failure with reduced coronary reserve.     

Ischemic preconditioning in the aged heart--myocardial protective effect as compared with the mature heart

It is now well established that pre-treatment with sublethal ischemia, followed by reperfusion, will delay myocardial necrosis during a later sustained ischemic episode, termed ischemic preconditioning (IPC); this has been confirmed experimentally and clinically. However, the effects for the senescent heart differ from those of the mature heart at both functional and cellular levels which have not yet been determined. Comparisons were made between aged (> 135 weeks, n = 18) and mature (15 approximately 20 weeks, n = 8) rabbit hearts which underwent 30 min. normothermic global ischemia with 120 min reperfusion in a buffer-perfused isolated, paced heart model, and the effects of IPC on post-ischemic functional recovery and infarct size were investigated. Ischemic preconditioned hearts (n = 6) were subjected to one cycle of 5 min. global ischemia and 5 min. reperfusion prior to global ischemia. Global ischemic hearts (n = 6) were subjected to 30 min. global ischemia without intervention. Control hearts (n = 6) were subjected to perfusion without ischemia. Post-ischemic functional recovery was better in the ischemic preconditioned hearts than in the global ischemic hearts in both aged and mature hearts. However, in the aged hearts, post-ischemic functional recovery was slightly reduced compared to that of the mature hearts, and only the coronary flow was well-preserved. In the mature hearts, myocardial infarction in the ischemic preconditioned hearts (14.9 +/- 1.3%) and in the control hearts (1.0 +/- 0.3%) was significantly decreased (p < 0.01) compared to that of the global ischemic hearts (32.9 +/- 5.1%). In the aged hearts, myocardial infarction in the ischemic preconditioned hearts (18.9 +/- 2.7%) and in the control hearts (1.1 +/- 0.6%) was significantly decreased (p < 0.001) compared to that of the global ischemic hearts (37.6 +/- 3.7%). The relationship between infarct size and post-ischemic functional recovery of left ventricularpeak developed pressure (LVDP) was linear and the correlation negative, with r = -0.934 (p < 0.001) and -0.875 (p < 0.001) for mature and aged hearts respectively. The data suggest that, in the senescent myocardium, the cellular pathways involved ischemic preconditioning responses that were post-ischemic, and that functional recovery was worse as compared to that of the mature myocardium. Furthermore, the effects of post-ischemic functional recovery became consistently weaker during the control period of 120 min. reperfusion after a prolonged ischemic insult in a buffer perfused isolated rabbit model. However, the effects of infarct size limitation were well-preserved in both senescent and mature myocardia.     

Factors modifying ischemic injury in the isolated rat heart

The extent of ischemic injury has been studied in the isolated working rat heart utilizing an aortic ball valve that reduces the coronary flow. A number of factors were tested including high heart rate, noradrenaline, acidosis, alkalosis, high afterload, beta-blockade, glucose-insulin-potassium (GIK), palmitate and methylprednisolone. Mechanical performance, myocardial contents of ATP, creatine phosphate, glycogen and lactate and the leakage of creatine phosphokinase (CK) from the myocardium to the perfusion buffer were measured and used for determination of the ischemic injury. Tachycardia, noradrenaline and palmitate are factors that markedly increase the ischemic injury in this preparation. GIK and probably metoprolol decrease the release of CK compared with the controls.     

Myocardial injury associated with potassium arrest

The relative efficacy of potassium-induced ischemic arrest using buffered, isosmotic potassium (25 mEq/liter) was compared with hypothermic arrest in an experimental protocol employing an intact canine heart preparation. Myocardial function (LVSW, dp/dt max), serum creatine phosphokinase levels, myocardial perfusion, and light and electron microscopical examination of the heart were assessed in five groups of 5 dogs each. There was one control group (90 minutes of bypass, no anoxia) and four experimental groups, each subjected to 1 hour of ischemic arrest and 30 minutes of reperfusion, comparing normothermic ischemic arrest (NIA), hypothermic ischemic arrest (myocardial temperature less than 25 degrees C) (HIA), normothermic potassium arrest (NKA), and hypothermic potassium arrest (HKA). Myocardial function decreased significantly following NIA and NKA but remained essentially equal in the control, HIA and HKA groups. Serum creatine phosphokinase analysis documented a significant increase in each group of animals: 2,250 mU after NIA, 1,778 mU after NKA, 1,388 mU after HIA, 1,220 mU after HKA, and 838 mU after control bypass. Left ventricular myocardial perfusion was unmeasurably low after NIA, reduced to 111 m/100 gm of tissue/min after NKA, and increased to 165 to 188 ml/100 gm/min in the control, HIA and HKA groups. Electron microscopical studies showed a range of myocardial changes, from probably irreversible damage after NIA to similar but less diffuse changes after NKA, and to potentially reversible changes after HKA and HIA with the least alteration from control after HIA. The results indicate that potassium arrest alone is not as effective as hypothermia in preventing ischemic injury, and the combination of hypothermia with a single 150 cc administration of potassium (25 mEq/liter) does not appear to provide significant additional protection.     

Heart failure as clinical onset of essential mixed cryoglobulinemia

The case of a 58-year old man affected by heart failure on ischemic basis, as clinical onset of essential mixed cryoglobulinemia (EMC) is reported. Laboratory assays, ECG at rest and exercise electrocardiogram, echocardiogram, myocardial scintigraphy, cardiac catheterization with coronarography, hepatic, bone and kidney biopsies confirmed the diagnosis. Cases of primitive heart involvement are rarely reported and are, usually, due to myocardial infarction. Nevertheless in the published series of cases, heart failure is often coupled with EMC and, not seldom, is the cause of death. In the present case heart failure was the dominant element of clinical symptomatology and wasn't consequent to renal involvement or hypertension, but was sustained by a myocardial contractile deficiency, on ischemic basis, with undamaged coronary circle at angiography. Therefore heart failure was ascribed to an involvement of coronary microcirculation in the course of systemic vasculitis.     

Renal stones and coronary heart disease

The relationship between risk factors for coronary heart disease (CHD) and renal stone disease has been studied in a population of more than 2000 middle-aged men. The only positive association found was a slight increase in diastolic BP among stone formers and a higher stone prevalence in untreated hypertensives. Furthermore, the prevalence of a history of renal stones in male survivors of myocardial infarction (MI) was similar to that found in the population study. An investigation of the vitamin D intake by means of a dietary questionnaire revealed no differences between stone formers, healthy controls and MI survivors. Contrary to other reports, the present study indicates that the risk factor profile for CHD in stone formers is similar to that in the general population.     

Myocardial damage after minimally invasive coronary artery bypass grafting on the beating heart

BACKGROUND: In conventional coronary artery bypass grafting, the rate of perioperative myocardial infarction is reported in the 2% to 6% range; however, significantly higher rates are observed if sensitive myocardial marker proteins are used to detect perioperative myocardial damage. For minimally invasive direct coronary artery bypass grafting, few data are available concerning myocardial marker protein release. METHODS: Fifteen consecutive patients (11 male, 4 female; mean age, 59.6 +/- 8.5 years) received minimally invasive direct coronary artery bypass grafting procedures via minithoracotomy on the beating heart. Electrocardiography and transesophageal and transthoracic echocardiography as well as determination of creatine kinase-MB mass concentration and cardiac troponin I level were used for ischemic monitoring. RESULTS: One patient had a perioperative myocardial infarction according to standard criteria and died despite mechanical circulatory support. Determination of cardiac troponin I level showed small but definitive ischemic damage in 4 of 9 patients (44%) who presented transient ischemic signs intraoperatively or postoperatively. In 2 of these 4 patients pathologic findings could be detected on angiographic restudies. CONCLUSIONS: Subclinical myocardial injury is a common event in minimally invasive coronary artery bypass grafting on the beating heart. Cardiac troponin I could serve as an adequate diagnostic tool for diagnosis of perioperative myocardial infarction in minimally invasive direct coronary artery bypass grafting.     

Imaging of myocardial perfusion and metabolism with positron emission tomography

Positron emission tomography (PET) has been providing new information in the diagnosis and the pathophysiological assessment of heart diseases. The PET tracers commonly used in Japan are 13N-ammonia, 18F-fluorodeoxyglucose (FDG) for imaging of myocardial perfusion and metabolism, respectively. Measurement of regional myocardial blood flow by 13N-ammonia dynamic PET scan and a compartment model analysis is applied to the functional estimation of coronary stenotic lesions and the detection of perfusion abnormalities in hypertrophic heart diseases, familial hyperchlesterolemia and other diseases with possible microvascular lesions. 18F-FDG is commonly used to differentiate ischemic but viable tissue from myocardial scar in coronary artery disease and also used to detect cardiac tumor and the cardiac involvement in sarcoidosis. In addition to these two tracers, 11C-acetate is now expected to provide the clinical analysis of pathophysiology of heart failure by estimating the efficiency of energy conversion of the heart into external work.     

Noninvasive stress testing of myocardial ischemia: comparison of GRE-MRI perfusion and wall motion analysis to 99 mTc-MIBI-SPECT, relation to coronary angiography

In the evaluation of ischemic heart disease only MR imaging seems to have the potential to assess myocardial perfusion, function, and coronary morphology on a single instrument. The aim of this study was to assess the feasibility of a stress test with dipyridamole (0. 56 mg/kg) to analyze myocardial perfusion by Gd first-pass enhancement in ultrafast gradient-recalled-echo MRI (perf-MRI), and wall motion by cine gradient-recalled-echo MRI (Cine-MRI) in one imaging session. Twelve patients underwent complete rest and stress studies; satisfactory MR images were acquired in 10 patients. By 99 mTc-MIBI-SPECT sensitivities to detect ischemic segments were 66.7 % with Perf-MRI, 80.0 % with WM-MRI and 86.7 % for Perf-WM-MRI (Perf-MRI vs Perf-WM-MRI; p = 0.03). Scar was equally detected with a sensitivity of 91.6 % with either MRI technique. Thus, Perf-Cine-MRI provides complementary information for the management of ischemic heart disease and has a higher sensitivity than Perf-MRI alone.     

Detection of hepatitis C virus RNA from the heart of patients with hypertrophic cardiomyopathy

We investigated hepatitis C virus (HCV) infection in 35 patients with hypertrophic cardiomyopathy and 40 patients with ischemic heart disease who were consecutively admitted to our hospital. Frequency of positive anti-HCV antibody was significantly higher in patients with hypertrophic cardiomyopathy (6 of 35 patients, 17.1%) than that in patients with ischemic heart disease (1 of 40 patients, 2.5%, p = 0.036). In three of these six patients with hypertrophic cardiomyopathy, HCV RNA was detected in myocardial tissue. In two of these three patients, HCV RNA was detected from biopsy and autopsy specimens of the ventricles, but not in the serum, suggesting that HCV may replicate in myocardial tissue and may be relevant to ventricular hypertrophy. Thus, HCV infection may play a role in the development of hypertrophic cardiomyopathy.     

Alteration of plasma antithrombin III levels in ischemic heart disease

The amount of antithrombin III in plasma was determined quantitatively in 218 males between 45-60 years of age. The mean antithrombin III value was found to be low in the group with low risk for ischemic heart disease, intermediate in the group with high risk for ischemic heart disease and highest in the group with acute myocardial infarction. Concomitant study of kaolin-activated partial thromboplastin time revealed a sharp decrease in its mean value in the group with acute myocardial infarction. The high correlation between antithrombin III and kaolin-activated partial thromboplastin time for the entire population suggests that the development of ischemic heart disease is a gradual process and that failure of the damping mechanism results as an acute event. These findings may be useful in the determination of the coagulation state of these patients.     

The effect of the mean platelet volume on the short-term prognosis of acute myocardial infarct

INTRODUCTION AND OBJECTIVES: The increase of mean platelet volume in the late phase of myocardial infarction is an independent predictor for recurrent myocardial infarction and death, but the association between this finding and the short-term prognosis after acute myocardial infarction is unknown. The goals of this study were to assess the influence of mean platelet volume on the risk of death, recurrent ischemic events or cardiac heart failure during the in-hospital phase of myocardial infarction and to analyse the relationship between mean platelet volume and several demographic and clinical variables registered on admission. MATERIAL AND METHODS: A population of 1,082 patients with acute myocardial infarction were distributed in two groups according to the platelet volume measured on admission: group 1, mean platelet volume > 9 fl (n = 443) and group 2, mean platelet volume < or = 9 fl (n = 639). The difference between both groups on the end-point of this study were assessed by univariate and multivariate statistical methods. An univariate analysis was also applied to assess the relationship between platelet volume and the baseline variables. RESULTS: A mean platelet volume > 9 fl was associated with a significant increase of risk for the combined end-point considered (OR = 1.37; p = 0.026). By univariate analysis, an increased platelet volume was related to a higher risk of cardiac failure (OR = 1.46; p = 0.01) and a non-significant increase in the incidence of recurrent ischemic events (OR = 1.35; p = 0.07). In addition, a large platelet volume was also associated with a higher prevalence of prior myocardial infarction, arterial hypertension and diabetes mellitus. CONCLUSIONS: The results of this study suggest that the increase of mean platelet volume on admission is an independent risk factor for cardiac heart failure and is associated with a non significant higher rates of ischemic events during the recovery phase of acute myocardial infarction.