Risk Of Sudden Coronary Death Research Articles

Risk of sudden coronary death based on genetic background in Chinese Han population.

Associations between gene variations and sudden cardiac arrest or coronary artery disease have been reported by genome-wide association studies. However, the implication of the genetic status in cases of sudden coronary death (SCD) from the Chinese Han population has remained to be investigated. The present study established a mini-sequencing system to examine putative death-causing single nucleotide polymorphisms (SNPs) using multiplex PCR, single base extension reaction and capillary electrophoresis techniques. A total of 198 samples from the Chinese Han population (age range, 34-71 years; mean age, 53.86 years) were examined using this method. Samples were classified into three groups: Coronary heart disease (CHD, n=70), SCD (n=53) and control (n=75) group. Significant associations were identified for 10, 4 and 6 SNPs in CHD, SCD and sudden death from CHD, respectively, using the χ2 test. The SNPs obtained by binary logistic regression may be used to assess and predict the risk of disease. The predictive accuracy of the SNPs in each prediction model and their area under the receiver operating characteristic curve (AUC) values were determined. The AUC of the four SNPs (rs12429889, rs10829156, rs16942421 and rs12155623) to predict CHD was 0.928, the AUC of the six SNPs (rs2389202, rs2982694, rs10183640, rs597503, rs16942421 and rs12155623) to predict SCD was 0.922 and the AUC of the four SNPs (rs16866933, rs4621553, rs10829156 and rs12155623) to predict sudden death from CHD was 0.912. The multifactor dimensionality reduction values were as follows: 0.8690 (prediction model of CHD), 0.7601 (prediction model of SCD) and 0.7628 (prediction model of sudden death from CHD). Taken together, the results of the present study suggested that these SNPs have considerable potential for application in genetic tests to predict CHD or SCD. However, further studies are required to investigate the putative functions of these SNPs.

Inducible Fast Ventricular Tachycardia After ST-Segment–Elevation Myocardial Infarction

Although our understanding of sudden cardiac death (SCD) is far from complete, at least part of SCD post–myocardial infarction (MI) is because of ventricular tachycardia (VT) that degenerates to ventricular fibrillation. Because of the poor outcome of resuscitative efforts, considerable effort has been directed at risk stratification to guide interventions to prevent and to protect patients from this syndrome. Several clinical and laboratory variables (structural, arrhythmic, and autonomic) have been associated with poor outcome; how to use these to determine which patients are likely to have SCD, for which we have an established primary prevention treatment strategy, versus non-SCD remains elusive. Article see p 884 Ventricular ectopy was first recognized as a predictor of death in 1969; ventricular ectopy recorded on a standard ECG in outpatients were associated with a 6-fold increase in sudden death.1 For patients with early post-MI, Lown et al2 postulated that an electric catastrophe is more likely when ventricular premature beats occur early in the cycle, in salvos of ≥2, when they are multiform, or with a frequency >5/min. Ruberman et al3 showed that complex premature beats were associated with a risk of sudden coronary death 3× that for men free of these findings. A graded prognostic importance of ventricular premature beats and left ventricular dysfunction was described in the Myocardial Post-Infarction Program.4 The risk of nonsustained VT lasting 4 to 7 beats in the setting of acute coronary syndromes persists today as shown in the Metabolic Efficiency with Ranolazine for Less Ischemia in Non-ST-elevation Acute Coronary Syndrome-Thrombolysis in Myocardial Infarction 36 (MERLIN-TIMI 36) study.5 Programmed electric stimulation (PES) arose as a way of mimicking spontaneous ectopy and subjecting it to formal study. The pioneering work of Wellens, Josephson and others suggested that inducibility indicated reentry as a mechanism of VT …

Acute myocardial infarction associated with ST segment elevation and the new European Society of Cardiology guidelines

Ischaemic heart disease is a major health problem in the western world. In many cases the first symptom of this disorder is acute myocardial infarction (AMI). The clinical spectrum of...

Abstract: 550 PLASMA TRIGLYCERIDE METABOLISM IN THE FED STATE – CLINICAL AND PATHOPHYSIOLOGICAL SIGNIFICANCE

In our recent report, it remained unclear whether or not triglyceride-rich lipoprotein remnants (RLP) were associated with the risk of sudden coronary death in younger cases without coronary atherosclerosis that were detected in about 10% of all sudden coronary death cases in Japan. These cases were categorized as ‘origin unknown, but suspected to be due to coronary spasm’, the so called ‘pokkuri disease’ in Japan. The present study population consisted of 108 sudden death cases without coronary atherosclerosis [(pokkuri disease n=57) and non-cardiac sudden death (control n=51)] aged 20–69 years from Kanagawa prefecture in Japan. All individuals had died suddenly and unexpectedly, most had no significant history of medical conditions including cardiac symptoms and had not taken medications prior to death according to their medical records. All the autopsies were performed within 12 h after death. Plasma total cholesterol (TC), triglycerides (TG), phospholipids, RLP-C and RLP-TG, VLDL-C, LDL-C, HDL-C, apolipoproteins A-I, A-II, B, C-II, C-III, E, Lp (a) and homocysteine were measured in postmortem plasma samples. The TG-rich lipoprotein remnants measured as RLP-C and RLP-TG were significantly higher in pokkuri disease compared with controls both in fasting and postprandial states (P<0.05 and P<0.001), indicating that RLP-C and RLP-TG were the most significant risk factor in pokkuri disease among the parameters tested in this study. In conclusion the TG level in RLP (RLP-TG) appeared to be strongly associated with the risk of sudden death in the absence of coronary atherosclerosis (pokkuri disease).

Long-term fish consumption and n-3 fatty acid intake in relation to (sudden) coronary heart disease death: the Zutphen study

To assess the relationship between fish consumption or eicosapentaenoic acid (EPA)+docosahexaenoic acid (DHA) intake from fish, and (sudden) coronary death. The impact of recent and long-term fish consumption and EPA+DHA intake on (sudden) coronary death was investigated in the Zutphen Study, a cohort of 1373 men born between 1900 and 1920, and examined repeatedly between 1960 and 2000. Hazard ratios were obtained from time-dependent Cox regression models. The associations between long-term fish consumption, EPA+DHA intake, and (sudden) coronary death were stronger than those of recent consumption. Long-term fish consumption was inversely associated (borderline significant) with coronary heart disease (CHD) death; however, the strength of the association decreased from age 50 [HR: 0.32 (95% CI: 0.13-0.80)] until age 80 [HR: 1.34 (0.58-3.12)]. For men with a daily EPA+DHA intake from fish below 250 mg compared with no intake, CHD death risk was reduced to the same extent as for men with a daily intake above 250 mg (P-value for trend: 0.27). Moreover, long-term fatty-fish consumption lowered the risk of sudden coronary death [HR: 0.46 (0.27-0.78)]. The strength of the association between long-term fish consumption and CHD death decreased with increasing age. Fatty-fish consumption lowered sudden coronary death risk. There was no clear dose-response relationship between EPA+DHA intake and (sudden) coronary death.

Factor V leiden, prothrombin g20210a, and risk of sudden coronary death in apparently healthy persons

nary saphenous venous grafts. Am J Cardiol 1995;75:26–29. 7. Jain SP, Liu MW, Dean LS, Babu R, Goods CM, Yadav JS, Al-Shaibi KF, Mathur A, Iyer SS, Parks JM, Baxley WA, Roubin GS. Comparison of balloon angioplasty versus debulking devices versus stenting in right coronary ostial lesions. Am J Cardiol 1997;79:1334–1338. 8. Zampieri P, Colombo A, Almagor Y, Maiello L, Finci L. Results of coronary stenting of ostial lesions. Am J Cardiol 1994;73:901–903. 9. Baldus S, Koster R, Elsner M, Walter DH, Arnold R, Auch-Schwelk W, Berger J, Rau M, Meinertz T, Zeiher AM, Hamm CW. Treatment of aortocoronary vein graft lesions with membrane-covered stents: a multicenter surveillance trial. Circulation 2000;102:2024–2027. 10. Briguori C, De Gregorio J, Nishida T, Adamian M, Albiero R, Tucci G, Di Mario C, Colombo A. Polytetrafluoroethylene-covered stent for the treatment of narrowings in aorticocoronary saphenous vein grafts. Am J Cardiol 2000;86:343– 346. 11. Baldus S, Koster R, Reimers J, Kahler J, Meinertz T, Hamm CW. Membranecovered stents: a new treatment strategy for saphenous vein graft lesions. Catheter Cardiovasc Interv 2001;53:1–4. 12. Kwok OH, Ng W, Chow WH. Late stent thrombosis after successful rescue of a major coronary artery rupture with a polytetrafluoroethylene-covered stent. J Invasive Cardiol 2001;13:391–394. 13. Campbell PG, Hall JA, Harcombe AA, de Belder MA. The Jomed Covered Stent Graft for coronary artery aneurysms and acute perforation: a successful device which needs careful deployment and may not reduce restenosis. J Invasive Cardiol 2000;12:272–276. 14. Ahmed JM, Hong MK, Mehran R, Mintz GS, Lansky AJ, Pichard AD, Satler LF, Kent KM, Wu H, Stone GW, Leon MB. Comparison of debulking followed by stenting versus stenting alone for saphenous vein graft aortoostial lesions: immediate and one-year clinical outcomes. J Am Coll Cardiol 2000;35:1560– 1568.

Plasma triglyceride-rich lipoprotein remnants as a risk factor of ‘Pokkuri disease’

In our recent report, it remained unclear whether or not triglyceride-rich lipoprotein remnants (RLP) were associated with the risk of sudden coronary death in younger cases without coronary atherosclerosis that were detected in about 10% of all sudden coronary death cases in Japan. These cases were categorized as ‘origin unknown, but suspected to be due to coronary spasm’, the so called ‘pokkuri disease’ in Japan. The present study population consisted of 108 sudden death cases without coronary atherosclerosis [(pokkuri disease n=57) and non-cardiac sudden death (control n=51)] aged 20–69 years from Kanagawa prefecture in Japan. All individuals had died suddenly and unexpectedly, most had no significant history of medical conditions including cardiac symptoms and had not taken medications prior to death according to their medical records. All the autopsies were performed within 12 h after death. Plasma total cholesterol (TC), triglycerides (TG), phospholipids, RLP-C and RLP-TG, VLDL-C, LDL-C, HDL-C, apolipoproteins A-I, A-II, B, C-II, C-III, E, Lp (a) and homocysteine were measured in postmortem plasma samples. The TG-rich lipoprotein remnants measured as RLP-C and RLP-TG were significantly higher in pokkuri disease compared with controls both in fasting and postprandial states ( P<0.05 and P<0.001), indicating that RLP-C and RLP-TG were the most significant risk factor in pokkuri disease among the parameters tested in this study. In conclusion the TG level in RLP (RLP-TG) appeared to be strongly associated with the risk of sudden death in the absence of coronary atherosclerosis (pokkuri disease).

Coronary atherosclerosis in unheralded sudden coronary death under age 50: histo-pathologic comparison with ‘healthy’ subjects dying out of hospital

Aim: sudden coronary death (SCD) in older individuals is generally associated with extensive coronary atherosclerosis, although it may be the first manifestation of ischaemic heart disease. In younger age-groups, SCD may occur in the presence of less severe disease. We sought to (1) examine the extent of coronary atherosclerosis in young victims of SCD compared with age- and sex-matched controls, (2) analyse the composition of atherosclerotic plaques in these patients, (3) identify the predominant mechanism of SCD, and (4) evaluate the possibility of detecting this mechanism on the basis of morphologic plaque features, in particular presence and amount of lipid accumulation and calcific deposits. Methods and results: coronary arteries were obtained at autopsy from 28 victims of SCD under age 50 with no prior clinical manifestation of ischaemic heart disease (IHD) and no myocardial scar formation and from 16 age- and sex-matched subjects dying of noncardiac causes out of hospital. Sections of all available major coronary arteries were cut in 5-mm intervals to yield a total of 1357 histologic sections, which were analysed using digitised planimetry. Victims of SCD had significantly more major coronary arteries per subject with luminal area narrowing ≥75% than controls (on average, 2.1 vs. 0.2). Plaque area per histologic section was 5.1±2.1 mm 2 in SCD cases and 2.0±0.9 mm 2 in controls ( P<0.001). The major constituent of all plaques was fibrous tissue. Lipid core area per section was 0.49±0.59 mm 2 in SCD cases and 0.004±0.01 mm 2 in controls ( P<0.001), and calcified plaque area was 0.18±0.19 mm 2 in SCD cases and 0.02±0.05 mm 2 in controls ( P<0.001), both defining significant differences between SCD cases and controls. Arterial thrombosis, most often with underlying plaque rupture was the mechanism of SCD in >80% of the cases. Considering histologic sections with ≥50 and with ≥75% area stenosis, plaque rupture was independently predicted by lipid core area. Calcific deposits were a frequent feature of plaque rupture but were only associated with it in univariate analysis. Conclusions: the extent and severity of coronary atherosclerosis in young victims of SCD as the first manifestation of IHD was substantially greater than in age-and sex-matched controls and comparable with that previously reported in SCD cases with a broader age range. Lipid core and calcified plaque areas provided for excellent separation between the two groups, which may have implications for identifying persons at increased risk for SCD by non invasive visualisation and assessment of the coronary arteries.

Effect of Antithrombotic Therapy on Risk of Sudden Coronary Death in Patients With Congestive Heart Failure

Data from epidemiologic, autopsy, Holter monitoring, and electrophysiologic studies support the hypothesis that acute myocardial ischemia, even in the absence of myocardial infarction, is a critical component of the pathophysiology of sudden coronary death. Acute myocardial ischemia superimposed upon ventricles damaged from previous infarctions has been demonstrated to enhance the generation of lethal ventricular arrhythmias. This is a retrospective analysis of 6,797 participants in the Studies of Left Ventricular Dysfunction prevention and treatment trials. Both univariate and multivariate Cox proportional-hazards modeling were used to study the association of anticoagulant and antiplatelet therapy with the risk for sudden cardiac death. The following covariates were adjusted for in the analysis: age, ejection fraction, gender, atrial fibrillation, diabetes, a history of angina, prior infarction, prior revascularization, and the regular use of beta blockers, diuretics, digoxin, antiarrhythmic agents, or enalapril. The overall incidence of sudden cardiac death per 100 patient-years of follow-up was 2.24%. In multivariate analysis, antiplatelet and anticoagulant monotherapy each remained independently associated with a reduction in the risk of sudden cardiac death: antiplatelet therapy with a 24% reduction (relative risk [RR] 0.76; 95% confidence interval [CI] 0.61–0.95) and antiplatelet monotherapy with a 32% reduction (RR 0.68; 95% CI 0.48–0.96). Thus, in patients with moderate to severe left ventricular systolic dysfunction resulting from coronary artery disease, antiplatelet and anticoagulant therapy are each associated with a reduction in the risk of sudden cardiac death.This is a retrospective database analysis of the Studies of Left Ventricular Dysfunction (SOLVD) prevention and treatment trials. We examined the association of antiplatelet and anticoagulant therapy with the risk for sudden cardiac death. In both univariate and multivariate analyses, both antiplatelet and anticoagulant therapy were each associated with a significant reduction in the risk for sudden cardiac death.

Sudden Out-of-Hospital Coronary Death in Patients with No Previous Cardiac History. An Analysis of 221 Patients Studied at Autopsy

Many epidemiological, clinical, and autopsy studies have demonstrated that the risk of sudden coronary death (SCD) is linked to the severity of coronary atherosclerotic lesions and to their thrombotic potential. However it remains unknown why some individuals manifest no clinical evidence of coronary disease until the onset of sudden death. The aim of this autopsy study has been to analyze the sociodemographic, clinical, and pathological features in case of sudden out-of-hospital coronary death where the death was the first manifestation of coronary disease. The results have been compared with those obtained from victims of SCD with known cardiac history. A total of 377 autopsies of sudden out-of-hospital cardiovascular deaths were performed at the Forensic Institute of Paris between 1989 and 1991. A total of 221 were SCD. A total of 160 of these subjects (72.4%) had no cardiac history (group A). The other 61 victims of SCD had cardiac antecedents (group B). Men account for 63% and 77% of the SCD in groups A and B respectively and are 12 years younger than women at the onset of SCD in both groups (65/77 years). Our study showed that in both groups SCD occurs in 83% of cases at home (and at rest) and in 30% of these cases while sleeping. Autopsy showed that SCD be it with or without antecedent occurs on a background of severe coronary disease with multivessels stenoses but coronary thrombosis was rarely observed (15%). SCD occurred in the context of underlying cardiomegaly.(ABSTRACT TRUNCATED AT 250 WORDS)

Reperfusion-induced arrhythmias and myocardial ion shifts: a pharmacologic interaction between pinacidil and cicletanine in isolated rat hearts.

Pinacidil is a member of the new antihypertensive drug family possessing an action that involves an increased potassium efflux in vascular and cardiac muscle. We investigated the contribution of opening of ATP-sensitive potassium channel to the development of reperfusion-induced arrhythmias and myocardial ion shifts, particularly that of Na+, K+, Ca2+, and Mg2+ in isolated rat hearts. After 30 min of normothermic global ischemia, pinacidil with 1 to 60 mumol/l failed to reduce the incidence of reperfusion-induced arrhythmias, even on the postischemic/reperfused myocardium in a subset of hearts unresponsive to reperfusion-induced arrhythmias (the duration of ischemia was reduced to 25 min), pinacidil treatment was associated with a greater incidence of reperfusion-induced arrhythmias (100%) as compared to the control value (50%). These proarrhythmic effects of pinacidil were also reflected in a maldistribution of myocardial ion contents both in nonischemic and ischemic/reperfused hearts. Cicletanine, a furopyridine antihypertensive agent that has no effect on coronary resistance, reduced the incidence of reperfusion arrhythmias, and its antiarrhythmic effect was antagonized by pinacidil. The same observation was made in relation to myocardial ion content, e.g., pinacidil-induced K+ loss and Ca2+ gain were antagonized by cicletanine, both in nonischemic and ischemic/reperfused hearts. It is hypothesized that the increased tendency to develop reperfusion-induced ventricular fibrillation is associated with the pinacidil-induced K+ efflux. The present study does not attempt to address the question of specific ionic currents; however, it has been suggested that proarrhythmic and antiarrhythmic effects of pinacidil and cicletanine, respectively, may relate to same receptor sites in which the latter may reflect a specific blockade of the outward K+ ion current via ATP-sensitive K+ channels. If this is so, the use of K+ channel openers as antihypertensive agents may be of particular concern in that population of postinfarction patients who are known to be at high risk of sudden coronary death.

Aortic calcified plaques and cardiovascular disease (the Framingham study)

The relation between the presence of calcified plaques in the thoracic aorta, as detected on chest x-rays, and the development of cardiovascular disease is examined during 12 years of follow-up of the Framingham cohort (n = 5,209). The prevalence of aortic calcified plaques approximately doubled with each decade of age, with only a trivial male predominance. Its presence was associated with a twofold increase in risk of cardiovascular death in men and women younger than age 65, even after other risk factors were taken into account. Similar increases in risk were found for coronary artery disease, stroke and intermittent claudication among middle-aged women. In middle-aged men these risks were less marked. The predictive value of aortic calcified plaques generally diminished with age. Risk of sudden coronary death in men with calcified plaques in the thoracic aorta ranged from a sevenfold increase at age 35 to no excess risk at age 70 years. These results support the view that atherosclerosis is a generalized process. The finding of aortic calcified plaques in a relatively young subject on a routine chest x-ray should be regarded as a sign for potential development of clinically manifest atherosclerotic disease in the cardiac, cerebral and peripheral arterial circulation.

Natural history of single vessel disease. Risk of sudden coronary death in relation to coronary anatomy and arrhythmia profile.

214 patients with single vessel disease were followed-up for 1-78 months (mean 48 months). Incidence of sudden death was studied in relation to coronary artery lesions, left ventricular wall motion and ventricular arrhythmias found during ambulatory ECG recording. Incidence of sudden death was 11% (16 of 144) in patients with lesions of the left anterior descending branch (LAD), 8% (4 of 55) in lesions of the right (RCA) and 7% (1 of 15) in those with lesions of the left circumflex (LCX) coronary artery. Coronary artery occlusion was associated with a significantly higher incidence of sudden death (15%, 18 of 123) than high-grade stenosis (3%, 3 of 91) (P less than 0.05). The risk of sudden death increased in patients with complex arrhythmias and occluded LAD or RCA (8 of 38, 21%; 2 of 12, 18%) compared with patients without complex arrhythmias (5 of 34, 15%; 1 of 18, 6%). One patient with LCX occlusion died suddenly. Our data show that the incidence of sudden death in relatively low in patients with single vessel disease. However, there is a high risk of sudden death in patients with LAD or RCA occlusion associated with akinetic left ventricular areas and complex arrhythmias.

Alcohol consumption and sudden coronary death in middle-aged Finnish men.

The association between consumption of alcoholic beverages (spirits, beer and wine) and coronary heart disease (CHD) mortality, especially the incidence of sudden coronary death (SCD), was investigated in a 5-year prospective population study comprising 4,532 men aged 40-64 years. The amount of alcohol used was estimated on the basis of answers to a self-filled structured questionnaire. The incidence of SCD was statistically significantly lower among abstainers than among alcohol consumers. The relative risk of SCD of alcohol consumers in comparison with abstainers was largest in the oldest age group and it became more apparent after a follow-up of a couple of years. Only the consumption of spirits was positively associated with the incidence of SCD. Among non-smokers the incidence of SCD was statistically significantly higher in consumers than in abstainers, a similar but not significant trend was observed among current smokers. The positive association between alcohol consumption and incidence of SCD was detected both in CHD-free men and in men with prior CHD. Consumption of alcoholic beverages, and in particular of spirits, is associated with an increased risk of SCD in Finnish men.

Implantable defibrillator electrode systems: a brief review.

Since the first report of a defibrillation attempt with an intracardiac catheter electrode nearly 30 years ago, investigators have developed implantable electrode systems consisting of metal disks, endocardial catheters, and epicardial patches. These early efforts demonstrated the feasibility of low-energy reversion of ventricular tachyarrhythmias, and also provided some insight into the mechanisms of fibrillation and defibrillation. This review describes the evolution of implantable defibrillator electrode systems. Early investigators attempted defibrillation with submuscularly implanted metal disks or a disk electrode paired with an endocardial catheter electrode. Electrode design emphasis turned to transvenous catheter systems with electrodes placed in the right ventricle and right atrium. A more successful configuration placed the proximal electrode in the superior vena cava. In an effort to ensure proper placement of the distal electrode in humans, the catheter was replaced with an epicardial patch. More recently, a combination of electrodes and multiple pulses has substantially reduced the energy required to defibrillate. Effective electrode systems that can convert lethal arrhythmias with a minimum of energy will aid in making implantable cardioverters and defibrillators the therapy of choice in patients at high risk of sudden coronary death.

Risk factors for sudden death after acute myocardial infarction: Two-year follow-up

The risk of sudden coronary death after myocardial infarction (MI) was assessed in 533 patients who survived 10 days after MI and were followed for up to 24 months (mean 18) in the Multicenter investigation of the Limitation of Infarct Size. Analysis of multiple clinical and laboratory variables determined before hospital discharge revealed that frequent ventricular premature beats (VPBs) (≥10/hpur) on ambulatory electrocardiographic monitoring and left ventricular (LV) dysfunction (radionuclide LV ejection fraction ≤0.40) were independently significant markers of risk for subsequent sudden death believed to be the result of a primary ventricular arrhythmia. The incidence of sudden death was 18% in patients with both LV dysfunction and frequent VPBs (11 times that of patients with neither of these findings). Seventy-nine percent of all sudden deaths occurred within 7 months after the index MI. In 280 survivors reclassified 6 months after MI with regard to the presence or absence of frequent VPBs and LV dysfunction, these risk factors could not be associated with sudden coronary death over a further follow-up period of up to 18 months; the overall incidence of sudden cardiac death was low (1.4%) after 6 months, thus, the presence of frequent VPBs in association with LV dysfunction early after MI identifies patients at high risk for sudden death over the next 7 months.

Ventricular premature complexes and sudden death after myocardial infarction.

Among 1739 male survivors of myocardial infarction, mortality over 5 years was examined in relation to presence of complex ventricular premature complexes (R on T, runs of two or more, multiform or bigeminal complexes) identified during 1 hour of monitoring. Such arrhythmia was associated with excess risk of death over the entire period. Men with R on T or runs during the hour show a 5-year sudden coronary death rate of 25%, compared with 6% of men free of premature complexes. Men with complex ventricular premature complexes are also at relatively higher risk for nonsudden cardiac death than the other men (5-year mortality 15% and 7%, respectively), but no additional disadvantage was associated with the presence of R on T or runs. Multivariate survival analyses, controlling simultaneously for other important clinical factors, identify complex ventricular premature complexes as the strongest influence on risk of sudden coronary death and congestive heart failure as the strongest influence on risk of other cardiac death.

Cardiovascular Diseases: An Annotated Bibliography of Recent Literature

Cardiovascular Diseases: An Annotated Bibliography of Recent Literature

Relation of education to sudden death after myocardial infarction.

We studied the influence of social and personal characteristics on prognosis among 1739 male survivors of myocardial infarction who had been monitored for one hour at a standard examination and subsequently followed for mortality. Over a three-year period men with little education (eight years of schooling or less) who had complex ventricular premature beats in the monitoring hour had over three times the risk of sudden coronary death found among better educated men with the same arrhythmia (cumulative mortality of 33 per cent and 9 per cent, respectively). No such differential appeared in the absence of complex ventricular premature beats. Neither risk factors for incidence of coronary heart disease nor clinical characteristics affecting prognosis accounted for the differences observed. There was no relation between education level and risk of recurrent infarction.

Ventricular premature beats and mortality after myocardial infarction.

To assess the role of ventricular premature beats in influencing mortality of coronary patients, 1739 men with prior myocardial infarction were monitored for ectopic activity for one hour at a standard base-line examination, and followed for mortality for periods up to four years (average, 24.4 months). Analyses of survival taking into account other important prognostic variables establish that the presence of complex premature beats (R on T, runs of 2 or more, multiform or bigeminal premature beats) in the monitoring hour is associated with a risk of sudden coronary death three times that of the men free of complex ventricular premature beats. The corresponding risk of death from any cause is twice that of men without such complex beats in the hour. These arrhythmias make an independent contribution to increased risk of death that persists over the length of this observation period.