Functional integrity of intrinsic cardiac nerves located over an acute transmural myocardial infarction

Acute transmural myocardial infarction has been reported to functionally denervate the normal myocardium distal to the infarcted zone by interrupting neurotransmission in axons coursing in the subepicardial region of the myocardial necrosis. To directly investigate the viability of such neurotransmission, the effects of acute transmural myocardial infarction on conduction in the intrinsic cardiac nerves overlying and distal to an experimentally induced acute transmural myocardial infarction were studied. In eight dogs, during control states electrical stimulation of the epicardium adjacent to a coronary artery produced compound action potentials in the more cranially located cardiopulmonary nerves. Thereafter, in four dogs an acute transmural myocardial infarction was produced by injecting rapidly hardening latex into a major diagonal branch of the left anterior descending coronary artery. Epicardial stimulation over the infarct, as well as proximal or distal to it, produced compound action potentials that conducted at normal velocities for at least 12 h postinfarction. The transmural extent of the infarct was verified with tetrazolium blue staining at the end of the experiment. In the other four dogs, compound action potentials were generated in cardiopulmonary nerves as described above and then ventricular fibrillation was produced to assess the effects of global anoxia on the function of axons coursing in cardiac nerves. Following the onset of ventricular fibrillation, compound action potentials were generated in these nerves in C fibers for up to 2 h, in B fibers for up to 4 h, and in A fibers for at least 12 h.(ABSTRACT TRUNCATED AT 250 WORDS)     

Chest pain in the early recognition of large infarcts.

Among 90 patients admitted to hospital with a diagnosis of first myocardial infarction consistent significant associations were found between pain duration, increase in concentration of serum glutamic oxaloacetic transminase (SGOT), maximum temperature and type of infarct (transmural or nontransmural). This suggests that infarct size may be associated with pain duration, increase in SGOT concentration and maximum temperature, and that patients with transmural infarcts have larger infarcts than those with nontransmural infarcts. A higher incidence of premonitory pain -- in particular, premonitory rest pain -- was noted in patients with transmural infarcts, who also had a significantly higher leukocyte count than patients with nontransmural infarcts. Pain intensity was also found to be associated directly with increase in SGOT concentration. However, because intergroup differences were not significant consistently, the association between infarct size, premonitory pain, pain intensity and leukocytosis is less certain. If the association between pain duration and infarct size is confirmed, a simple means would be available for the early recognition of the patient with a large infarct and adverse prognosis who would benefit from prompt therapeutic measures to reduce infarct size.     

63例非典型急性下壁心肌梗死临床分析

目的：研究评价各种常见诱因对急性下壁心肌梗死（IAMI）患者误诊判断的临床意义。方法：选择2002年1月-2009年12月我院急门诊IAMI患者63例,对其首发症状、心电图资料进行回顾性分析。结果：63例中,以头晕乏力首诊19例（30．16％）,以晕厥首诊11例（17．46％）,以上腹痛伴恶心呕吐,偶腹泻首诊13例（20．63％）,以咽痛或牙痛首诊10例（15．87％）,以呼吸困难首诊8例（12．70％）,以左心衰竭首诊2例（3．17％）。结论：对急性下壁心肌梗死患者,常规心电图检查是必要的。再结合心肌坏死生化标志物指标,早诊断,早治疗。     

Reduction of ventricular arrhythmias by early intravenous atenolol in suspected acute myocardial infarction.

The effect of intravenous atenolol on ventricular arrhythmias in acute myocardial infarction was assessed in 182 patients admitted within 12 hours of the onset of chest pain. Ninety-five patients were randomised to receive 5 mg intravenous atenolol followed immediately by 50 mg by mouth and 50 mg 12 hours later, then 100 mg daily for 10 days; 87 patients served as controls. The treated patients had significantly fewer ventricular extrasystoles; 58 control patients (67%) had R-on-T extrasystoles compared with only 25 treated patients (26%) (2p less than 0.0001); repetitive ventricular arrhythmias were detected in 64 control patients (74%) and 55 treated patients (58%) (2p less than 0.05). Heart rate was significantly reduced from 77 +/- 1 beats/min at entry to 65 +/- 1 beats/min (2p less than 0.001) in the first hour after intravenous atenolol, and in addition the rate was significantly different from that in the control group. There was no difference in the incidence of heart failure, but fewer patients in the treated group received other antiarrhythmic agents or digoxin. These results show that early intravenous atenolol prevents ventricular arrhythmias in suspected acute myocardial infarction.     

A comparison of aspirin and anticoagulation following thrombolysis for myocardial infarction (the AFTER study): a multicentre unblinded randomised clinical trial.

OBJECTIVE: To compare aspirin with anticoagulation with regard to risk of cardiac death and reinfarction in patients who received anistreplase thrombolysis for myocardial infarction. DESIGN: A multicentre unblinded randomised clinical trial. SETTING: 38 hospitals in six countries. SUBJECTS: 1036 patients who had been treated with anistreplase for myocardial infarction were randomly assigned to either aspirin (150 mg daily) or anticoagulation (intravenous heparin followed by warfarin or other oral anticoagulant). The trial was stopped earlier than originally intended because of the slowing rate of recruitment. MAIN OUTCOME MEASURE: Cardiac death or recurrent myocardial infarction at 30 days. RESULTS: After 30 days cardiac death or reinfarction, occurred in 11.0% (57/517) of the patients treated with anticoagulation and 11.2% (58/519) of the patients treated with aspirin (odds ratio 1.02, 95% confidence interval 0.69 to 1.50, P = 0.92). Corresponding findings at three months were 13.2% (68/517) and 12.1% (63/519) (0.91, 0.63 to 1.32, P = 0.67). Patients receiving anticoagulation were more likely than patients receiving aspirin to have had severe bleeding or a stroke by three months (3.9% v 1.7% (0.44, 0.20 to 0.97, P = 0.04)). CONCLUSION: No evidence of a difference in the incidence of cardiac events was found between the two treatment groups, though the trial is too small to claim treatment equivalence confidently. A higher incidence of severe bleeding events and strokes was detected in the group receiving anticoagulation, suggesting that aspirin may be the drug of choice for most patients in this context.     

Long-term beta blockade: possible protection from myocardial infarction.

The clinical behaviour of 90 patients on beta-blocking drugs for established coronary heart disease who were admitted to a coronary care unit with prolonged ischaemic myocardial pain was compared with that of 90 similar patients not on this therapy. Transmural myocardial infarction was confirmed in 30 of the patients on beta-blockers and in 62 controls. A diagnosis of myocardial necrosis without infarction was made in 20 patients on beta-blockers and in 14 controls. Coronary insufficiency was diagnosed in 40 patients on beta-blockers and in 14 controls. The incidence of simus bradycardia, hypotension, syncope, and radiological pulmonary oedema was similar in the two groups. Established beta-blockade, therefore, has not been shown to prejudice the outcome of patients with coronary heart disease admitted to hospital with prolonged ischaemic myocardial pain. On the contrary, it may protect some patients from the development of a myocardial infarction.     

Cardiac arrhythmias in myocardial infarction as an extension of lesions to the myocardium and the state of circulatory efficiency

The study involved 55 patients with the acute myocardial infarction aged between 34 and 69 years (mean 53 years) in whom the relation of cardiac arrhythmias incidence to the extension of myocardial involvement and circulatory efficiency was assessed. All patients were examined clinically, a 24-hour ECG with Holter technique (in the first day, 21st day and 6th months after myocardial infarction) and echocardiographic (Echo-2D) tests were registered. Echocardiography was performed during hospital phase and 6 months after myocardial infarction. Cardiac arrhythmias were evaluated with classification into classes described by Lown. Close relation of serious cardiac arrhythmias with extension of myocardial involvement was noted especially in the acute phase of myocardial infarction. High risk arrhythmias--class IVA, IVB and V were noted in nearly 100% of patients in this phase with cardiac aneurysm, extensive akinesis of apex and anterior wall of the heart. Mean value of the ejection fraction was 31% in this group. Incidence of cardiac arrhythmias did not exceed 40%, ejection fraction was 56% in the group of patients with limited lesions to the heart, e.g. akinesis of the lower wall. Incidence of late cardiac arrhythmias (6 months) did not differ significantly in particular groups of patients. The value of ejection fraction remained, however, on the same level as in the hospital phase of the myocardial infarction.     

The x-ray picture of pulmonary circulation in the course of acute myocardial infarct

A study was made of the time course of lesser circulation (LC) in 80 patients with acute transmural myocardial infarction and in 20 patients with chronic coronary heart disease with the help of chest x-ray. A possibility of preclinical detection of left ventricular insufficiency was confirmed. The capacity of roentgenography to reflect objectively the time course of LC disorder and its correlation with primary determination of a degree of changes, age, cardiac sizes, the expression of aortic atherosclerosis, pleurocardiac reactions and site of myocardial infarction were defined.     

Prospective study of the role of cardiac troponin T in patients admitted with unstable angina.

OBJECTIVE--To examine the prognostic significance and role in risk stratification of the biochemical marker troponin T in patients admitted with unstable angina. DESIGN--Single centre, blinded, prospective study of patients admitted with chest pain. SETTING--Coronary care unit of a district general hospital. SUBJECTS--460 patients admitted with chest pain and followed up for a median of three years. 183 patients had a final diagnosis of unstable angina. MAIN OUTCOME MEASURES--Cardiac death, need for coronary revascularisation, or readmission with non-fatal myocardial infarction as first events. RESULTS--62 (34%) unstable angina patients were troponin T positive. This group had significantly increased incidence rates of subsequent cardiac death (12 cases (19%) v 14 (12%)), coronary revascularisation (22 (35%) v 26 (21%)), death or revascularisation (33 (53%) v 40 (33%)), and death or non-fatal myocardial infarction (18 (29%) v 21 (17%)) compared with the troponin T negative group. In multiple logistic regression troponin T status was a highly significant predictor for the end points coronary revascularisation and cardiac death or revascularisation as first events. CONCLUSION--Troponin T in the serum of patients with unstable angina identifies a subgroup at higher risk of subsequent cardiac events and its measurement aids in risk factor stratification. The increased risk extends to two years after admission. Prospective randomised trials are required to identify optimum therapeutic strategies for this subgroup.     

纤维蛋白原与冠心病PCI介入治疗围术期心肌梗死的相关性

目的:探讨纤维蛋白原与冠心病介入治疗围术期心肌梗死的相关性。方法:2013年1月到2015年1月,选择在我院进行诊治的冠心病患者92例,都给予PCI介入手术治疗,在手术前后进行纤维蛋白原与心功能的测定,对围术期心肌梗死发生情况与临床资料进行调查与分析。结果:所有患者都介入手术治疗成功,术后LVESVI与LVEDVI值都明显低于术前(P0.05),而术后LVEF值明显高于术前(P0.05);术后患者的血浆纤维蛋白原值为3.66±0.42 g/L,明显低于术前的7.45±0.56 g/L(P0.05)。围手术期发生心肌梗死8例,发生率为8.7%。Spearman秩相关分析法结果显示心肌梗死发病与血浆纤维蛋白原、LVESVI、LVEDVI、LVEF值都存在明显相关性(P0.05),多元Logistic回归分析结果显示纤维蛋白原、LVESVI、LVEDVI、LVEF、年龄为导致冠心病围术期心肌梗死的主要危险因素(P0.05)。结论:介入手术治疗冠心病具有很好的效果,但是围术期心肌梗死的发生率比较高,纤维蛋白原能有效反应病变状况,在心肌梗死的发生发展中起着关键性作用。     

MYOCARDIAL INFARCTION FOLLOWING CAROTID ENDARTERECTOMY

Myocardial infarction has been the major cause of mortality following operation for cerebrovascular insufficiency. In our institution, a clinical diagnosis of coronary artery disease was made in 37 of 125 (29.6%) consecutive male patients having carotid endarterectomy. Six of these 37 patients developed postoperative myocardial infarction. In contrast, none of the 88 patients without coronary artery disease developed myocardial infarction. A more recently treated group of 20 patients who had undergone carotid artery surgery and had previously undergone coronary artery bypass for angina did not develop postoperative myocardial infarction. These data suggest that in patients with both coronary artery and carotid artery disease, prior or concomitant coronary artery bypass should be considered. Myocardial infarction has been the leading cause of early and late death following operation for cerebrovascular insufficiency.(1) DeBakey(2) found operative mortality in patients having surgery for cerebrovascular insufficiency directly related to the incidence of coronary artery disease. An increased operative mortality due to reinfarction has been found in patients recovering from recent myocardial infarction.(3) Cooley(4) found that in patients having aortocoronary bypass there was no increased operative mortality 30 days after myocardial infarction and this may apply to patients having carotid endarterectomy. Subendocardial postoperative infarction associated with minor T wave changes and slight enzyme elevation had a better prognosis than did transmural infarction causing significant Q waves, sequential ST and T wave changes and marked enzyme elevations.(5) The purpose of this study was to document our experience with myocardial infarction in patients undergoing carotid artery operation for clinical coronary artery disease. Consideration of the role of saphenous vein bypass in those patients with coronary artery disease was the background for this review even though the evidence that myocardial infarction can be prevented with saphenous vein bypass operation is only preliminary at the present time.(6)     

Influence of oral magnesium supplementation on cardiac events among survivors of an acute myocardial infarction.

OBJECTIVE--To investigate the effect of long term oral magnesium treatment on incidence of cardiac events among survivors of an acute myocardial infarction. DESIGN--Double blind, placebo controlled parallel study in which patients were randomised to treatment or placebo. SETTING--Two coronary care units and corresponding outpatient clinics. SUBJECTS--468 survivors of an acute myocardial infarction (289 men and 178 women) aged 31-92. INTERVENTIONS--One tablet of 15 mmol magnesium hydroxide or placebo daily for one year. MAIN OUTCOME MEASURES--Incidences of reinfarction, sudden death, and coronary artery bypass grafting in one year. RESULTS--There was no significant difference between treatment and placebo groups in the incidence of each of the three cardiac events, but when the events were combined and drop outs were excluded from calculations there was a significantly higher incidence of events in the treatment group (56/167 v 33/153; relative risk 1.55 (95% confidence interval 1.07 to 2.25); p = 0.02). When the timing of events was incorporated by means of a Kaplan-Meier plot the treatment group showed a significantly higher incidence of events whether drop outs were included or excluded (p < 0.025). CONCLUSION--Long term oral treatment with 15 mmol magnesium daily doses not reduce the incidence of cardiac events in survivors of an acute myocardial infarction and, indeed, seems to increase the risk of developing a cardiac event. Consequently, this treatment cannot be recommended as secondary prophylaxis for such patients.     

Risks and benefits of aortocoronary bypass surgery in patients aged 65 years or more.

Between January 1970 and July 1978, 85 patients aged 65 years or more underwent aortocoronary bypass surgery at the Montreal Heart Institute. The mortality during the operation and the first 29 days thereafter was 12% overall, but was only 5% when the myocardium was protected by the use of cold cardioplegic solutions. Of the 75 patients who survived this period 7 (9%) had a perioperative transmural myocardial infarction. Nonfatal noncardiac complications were more common in these patients than in younger patients, but did not lead to permanent deficits. Three patients died after discharge from hospital, two of cardiac causes. Only one patient had a nonfatal myocardial infarction after discharge. The actuarial 5-year survival rate for all the patients was 80%. After a mean follow-up period of 30 months the condition of 94% of the patients was improved by at least one class of the New York Heart Association functional classification, and 68% were asymptomatic. It is concluded that aortocoronary bypass surgery can be performed in selected older patients with a relatively low in-hospital mortality and morbidity. Symptomatic improvement occurs in almost all such patients. Cardiac catheterization and aortocoronary bypass surgery should therefore be performed in selected older patients with severe angina that is refractory to optimum medical therapy.     

Immunoscintigraphy for detecting acute myocardial infarction without electrocardiographic changes.

OBJECTIVE--To establish whether immunoscintigraphy with antibody to myosin may detect acute myocardial infarction without electrocardiographic changes. DESIGN--Prospective study of patients with suspected acute myocardial infarction or unstable angina with cardiac imaging with 111indium myosin antibody, estimation of cardiac enzyme concentrations, electrocardiography, 201thallium imaging, and radionuclide ventriculography. SETTING--Coronary care unit in a district general hospital. PATIENTS--119 Consecutive patients with suspected acute myocardial infarction or unstable angina. Patients with cardiomyopathy, myocarditis, valvular heart disease, myocardial infarction or cardiac surgery in the previous two weeks or with left bundle branch block and women of childbearing age were excluded. RESULTS--Of 75 patients with suspected acute myocardial infarction, seven had no diagnostic electrocardiographic changes despite normal conduction patterns. Immunoscintigraphy with myosin antibody disclosed necrosis in all seven patients, which was localised in regions supplied by diseased coronary arteries in all but one. Six patients had abnormal images on 201thallium imaging, and all seven had abnormal wall motion at the site of antibody uptake. One patient with minimal left main stem and right coronary artery atheroma had uptake of antibody at two discrete sites. CONCLUSIONS--Immunoscintigraphy with antibody to myosin confirms myocardial infarction in the absence of electrocardiographic changes and discloses the site of infarction.     

Influence of environmental stress on pathogenesis of sudden cardiac death.

The effects of 20th-century stress on the cardiovascular system are reviewed and correlated with experimental animal models. A classic example of such stress is drawn from a study of the aerospace workers at Cape Kennedy who were shown to be exposed to excessive occupational stress. Surprisingly, the usual risk factors did not predict a greater risk, yet the population exhibited a higher incidence of sudden cardiac death and acute myocardial infarction. Acute myocardial necrosis was much more frequently demonstrated than was acute coronary obstruction of any type. Retrospective coroner's studies revealed two types of myocardial necrosis: 1) elongated, thinned or wavy fibers and 2) anomalous contraction bands. Correlation of these clinical observations with experimental data was duplicated in canine models of myocardial infarcion and/or catecholamine-induced necrosis. Catecholamines can lead to irreversible myocardial necrosis but the underlying mechanisms appear to be complex. Extrapolation of the results from the experimental and clinical studies suggests that environmental stress can lead to myocardial necrosis.     

急性心肌梗死患者心电图碎裂QRS波与左心室收缩功能、心率变异性及心脏事件的关系研究

目的:探讨急性心肌梗死患者心电图碎裂QRS(f QRS)波与左心室收缩功能、心率变异性及心脏事件的关系。方法:收集2018年1月～2020年1月期间于本院进行治疗的急性心肌梗死患者124例,对患者行心电图检查,根据患者心电图是否出现f QRS波分成f QRS组(59例)和无f QRS组(65例),采用多普勒超声诊断仪对两组患者的左心室收缩功能进行检测对比,并对两组患者进行24h动态心电图检查,对两组患者的心率变异性指标进行统计对比。对两组患者进行为期3个月的随访观察,统计对比两组患者随访期间心脏事件的发生率。结果:f QRS组患者的左室射血分数(LVEF)低于无f QRS组,左心室舒张末期容积(LVEDV)、左心室舒张末期内径(LVEDD)均高于无f QRS组(P0.05)。f QRS组患者总标准差(SDNN)、两个相邻RR间期互差(PNN50)、差值均方根(RMSSD)均低于无f QRS组(P0.05)。随访期间f QRS组患者的心脏事件发生率为35.59%(21/59),高于无f QRS组患者的13.85%(9/65)(P0.05)。结论:伴有心电图f QRS波急性心肌梗死患者的左心室收缩功能降低,心率变异性指标降低,且心脏不良事件发生率增加,心电图f QRS波在一定程度上可作为急性心肌梗死患者心功能、心率变异性及心脏事件发生的监测手段。     

负荷量阿托伐他汀对稳定型冠心病患者非心脏手术围手术期保护作用的研究

目的:探讨负荷量阿托伐他汀对稳定型冠心病患者非心脏的择期外科手术围手术期主要不良心脏事件的保护作用。方法:将拟行非心脏外科手术的60名稳定型冠心病患者随机分为负荷量阿托伐他汀组(n=30)和对照组(n=30),其中负荷量阿托伐他汀治疗组在术前12小时给予阿托伐他汀80 mg顿服,术前2小时阿托伐他汀40 mg顿服,且每晚服用阿托伐他汀40 mg,对照组术前每晚服用阿托伐他汀20 mg,而后进行非心脏的外科手术(主要病种为慢性胆囊结石胆囊炎、慢性阑尾炎、消化性溃疡、疝气),术后负荷量组给予每晚服用阿托伐他汀40 mg,对照组每晚服用阿托伐他汀20 mg。比较两组围手术期主要不良心脏事件(包括心脏性猝死,急性心肌梗死,非计划性血运重建)的发生情况。结果:对照组出现1例急性前壁ST段抬高型心肌梗死并行急诊前降支介入再灌注治疗和7例无症状型心肌梗死,负荷量阿托伐他汀组出现1例无症状型心肌梗死,围手术期心肌梗死发生率较对照组明显降低(P0.05)。结论:负荷量阿托伐他汀可显著降低稳定型冠心病患者非心脏的择期外科手术围手术期主要不良心脏事件如心肌梗死,特别是无症状型心肌梗死的发生率,但该结果尚需大样本多中心随机对照临床试验进一步证实。     

Comparison of NOGA Endocardial Mapping and Cardiac Magnetic Resonance Imaging for Determining Infarct Size and Infarct Transmurality for Intramyocardial Injection Therapy Using Experimental Data

Objectives

We compared the accuracy of NOGA endocardial mapping for delineating transmural and non-transmural infarction to the results of cardiac magnetic resonance imaging (cMRI) with late gadolinium enhancement (LE) for guiding intramyocardial reparative substance delivery using data from experimental myocardial infarction studies.

Methods

Sixty domestic pigs underwent diagnostic NOGA endocardial mapping and cMRI-LE 60 days after induction of closed-chest reperfused myocardial infarction. The infarct size was determined by LE of cMRI and by delineation of the infarct core on the unipolar voltage polar map. The sizes of the transmural and non-transmural infarctions were calculated from the cMRI transmurality map using signal intensity (SI) cut-offs of>75% and>25% and from NOGA bipolar maps using bipolar voltage cut-off values of <0.8 mV and <1.9 mV. Linear regression analysis and Bland-Altman plots were used to determine correlations and systematic differences between the two images. The overlapping ratios of the transmural and non-transmural infarcted areas were calculated.

Results

Infarct size as determined by 2D NOGA unipolar voltage polar mapping correlated with the 3D cMRI-LE findings (r = 0.504, p<0.001) with a mean difference of 2.82% in the left ventricular (LV) surface between the two images. Polar maps of transmural cMRI and bipolar maps of NOGA showed significant association for determining of the extent of transmural infarction (r = 0.727, p<0.001, overlap ratio of 81.6±11.1%) and non-transmural infarction (r = 0.555, p<0.001, overlap ratio of 70.6±18.5%). NOGA overestimated the transmural scar size (6.81% of the LV surface) but slightly underestimated the size of the non-transmural infarction (−3.04% of the LV surface).

Conclusions

By combining unipolar and bipolar voltage maps, NOGA endocardial mapping is useful for accurate delineation of the targeted zone for intramyocardial therapy and is comparable to cMRI-LE. This may be useful in patients with contraindications for cMRI who require targeted intramyocardial regenerative therapy.     

Diagnostic re-classification and prognostic risk stratification of patients with acute chest pain

Unstable angina and myocardial infarction are prevalent manifestations of acute coronary artery disease, combined in the term ‘acute coronary syndromes’. The introduction of sensitive markers for myocardial necrosis has led to confusion regarding the distinction between small myocardial infarctions and ‘true’ unstable angina, and the application of ever more sensitive markers has accelerated the pace at which patients with unstable angina are being re-classified to non-ST-segment elevation myocardial infarction. But in how many patients with acute chest pain is myocardial ischaemia really the cause of their symptoms? Numerous studies have shown that most have <5 ng/l high-sensitivity cardiac troponin, and that their prognosis is excellent (event rate <0.5% per year), incompatible with ‘impending infarction’. This marginalisation of patients with unstable angina pectoris should lead to the demise of this diagnosis. Without unstable angina, the usefulness of the term acute coronary syndromes may be questioned next. It is better to abandon the term altogether and revert to the original diagnosis of thrombus-related acute coronary artery disease, myocardial infarction. A national register should be the next logical step to monitor and guide the application of effective therapeutic measures and clinical outcomes in patients with myocardial infarction.

     

Shortened bleeding time in acute myocardial infarction and its relation to platelet mass.

The bleeding time, using the Simplate method, horizontal incision, and venostasis, was measured in a study of 51 patients admitted to a coronary care unit within 12 hours of the onset of chest pain. The bleeding time was significantly shorter in the 28 patients who were found to have definite myocardial infarction compared with the 23 others with chest pain but no definite infarction (p less than 0.0005). A bleeding time of less than 212 seconds correctly classified 84% of patients (sensitivity for definite myocardial infarction 89%) presenting to the coronary care unit with chest pain. Multiple regression analysis showed the bleeding time in all patients to be determined independently (and with high significance) by the following variables in order of importance: diagnostic group, platelet mass (platelet count X mean volume), and age. Packed cell volume was not a significant determinant. In the group with definite myocardial infarction considered alone the same order of variables was observed in predicting bleeding time, but none of them was significant. A major variable reducing bleeding time in acute myocardial infarction remains to be determined. There was no association between bleeding time and creatine phosphokinase activity or infarct size in the group with definite myocardial infarction.