Number Of Major Coronary Arteries Research Articles

High-Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long-Term Outcomes.

BackgroundThe associations between high‐sensitivity troponin I (hsTnI) levels and coronary artery disease (CAD) severity and progression remain unclear. We investigated whether there is an association between hsTnI and angiographic severity and progression of CAD and whether the predictive value of hsTnI level for incident cardiovascular outcomes is independent of CAD severity.Methods and ResultsIn 3087 patients (aged 63±12 years, 64% men) undergoing cardiac catheterization without evidence of acute myocardial infarction, the severity of CAD was calculated by the number of major coronary arteries with ≥50% stenosis and the Gensini score. CAD progression was assessed in a subset of 717 patients who had undergone ≥2 coronary angiograms >3 months before enrollment. Patients were followed up for incident all‐cause mortality and incident cardiovascular events. Of the total population, 11% had normal angiograms, 23% had nonobstructive CAD, 20% had 1‐vessel CAD, 20% had 2‐vessel CAD, and 26% had 3‐vessel CAD. After adjusting for age, sex, race, body mass index, smoking, hypertension, diabetes mellitus history, and renal function, hsTnI levels were independently associated with the severity of CAD measured by the Gensini score (log 2 ß=0.31; 95% confidence interval, 0.18–0.44; P<0.001) and with CAD progression (log 2 ß=0.36; 95% confidence interval, 0.14–0.58; P=0.001). hsTnI level was also a significant predictor of incident death, cardiovascular death, myocardial infarction, revascularization, and cardiac hospitalizations, independent of the aforementioned covariates and CAD severity.ConclusionsHigher hsTnI levels are associated with the underlying burden of coronary atherosclerosis, more rapid progression of CAD, and higher risk of all‐cause mortality and incident cardiovascular events. Whether more aggressive treatment aimed at reducing hsTnI levels can modulate disease progression requires further investigation.

Atherosclerotic Burden and Heart Failure After Myocardial Infarction.

Whether the extent of coronary artery disease (CAD) is associated with the occurrence of heart failure (HF) after myocardial infarction (MI) is not known. Furthermore, whether this association might differ by HF type according to preserved or reduced ejection fraction (EF) has yet to be determined. To evaluate in a community cohort of patients with incident (first-ever) MI the association of angiographic CAD with subsequent HF and to examine the prognostic role of CAD according to HF subtypes: HF with reduced EF and HF with preserved EF. A population-based cohort study was conducted in 1922 residents of Olmsted County, Minnesota, with incident MI diagnosed between January 1, 1990, and December 31, 2010, and no prior HF; study participants were followed up through March 31, 2013. The extent of angiographic CAD was determined at baseline and categorized according to the number of major epicardial coronary arteries with 50% or more lumen diameter obstruction. The primary end point was time to incident HF. The primary exposure variable was the extent of CAD as expressed by the number of major coronary arteries with significant obstruction (0-, 1-, 2-, or 3-vessel disease) obtained from coronary angiograms performed no more than 1 day after the MI. Heart failure was ascertained by the Framingham criteria and classified by type according to EF (50% cutoff). Of the 1922 participants, 1258 (65.4%) were men (mean [SD] age, 64 [13] years). During a mean follow-up period of 6.7 (5.9) years, 588 patients (30.6%) developed HF. With death and recurrent MI modeled as competing risks, the cumulative incidence rates of post-MI HF among patients with 0 or 1, 2, and 3 diseased vessels were 10.7%, 14.6%, and 23.0% at 30 days; and 14.7%, 20.6%, and 29.8% at 5 years, respectively (P < .001 for trend). After adjustment for clinical characteristics in a Cox proportional hazards regression model, the hazard ratios (95% CIs) for HF were 1.25 (0.99-1.59) and 1.75 (1.40-2.20) in patients with 2 and 3 vessels vs 0 or 1 occluded vessel, respectively (P < .001 for trend). The increased risk with a greater number of occluded vessels was independent of the occurrence of a recurrent MI and did not differ appreciably by HF type. The extent of angiographic CAD is an indicator of post-MI HF regardless of HF type and independent of recurrent MI. These data underscore the need to further investigate the processes taking place in the transition from myocardial injury to HF.

Prognostic importance of coronary anatomy and left ventricular ejection fraction despite optimal therapy: Assessment of residual risk in the Clinical Outcomes Utilizing Revascularization and Aggressive DruG Evaluation Trial

It is unknown if baseline angiographic findings can be used to estimate residual risk of patients with chronic stable angina treated with both optimal medical therapy (OMT) and protocol-assigned or symptom-driven percutaneous coronary intervention (PCI). Death, myocardial infarction (MI), and hospitalization for non-ST-segment elevation acute coronary syndrome were adjudicated in 2,275 COURAGE patients. The number of vessels diseased (VD) was defined as the number of major coronary arteries with ≥50% diameter stenosis. Proximal left anterior descending, either isolated or in combination with other disease, was also evaluated. Depressed left ventricular ejection fraction (LVEF) was defined as ≤50%. Cox regression analyses included these anatomical factors as well as interaction terms for initial treatment assignment (OMT or OMT + PCI). Percutaneous coronary intervention and proximal left anterior descending did not influence any outcome. Death was predicted by low LVEF (hazard ratio [HR] 1.86, CI 1.34-2.59, P < .001) and VD (HR 1.45, CI 1.20-1.75, P < .001). Myocardial infarction and non-ST-segment elevation acute coronary syndrome were predicted only by VD (HR 1.53, CI 1.30-1.81 and HR 1.24, CI 1.06-1.44, P = .007, respectively). In spite of OMT and irrespective of protocol-assigned or clinically driven PCI, LVEF and angiographic burden of disease at baseline retain prognostic power and reflect residual risk for secondary ischemic events.

Abstract 681: Characteristics of Atherosclerotic Plaque Burden in Patients With and Without Acute Coronary Syndrome Presenting With Acute Chest Pain to the Emergency Department

Background: Coronary computed tomography (CT) may improve the early triage of patients with acute chest pain in the emergency department (ED). The aim of this study was to compare the presence and extent of coronary atherosclerotic plaque as detected by coronary CT in patients with and without acute coronary syndromes (ACS). Methods: The study was designed as a prospective, observational cohort study in patients with acute chest pain but negative cardiac biomarkers and no diagnostic ECG changes, admitted to rule out myocardial ischemia. All patients underwent coronary CT prior to hospital admission. The presence of coronary plaque was treated as a dichotomous outcome, and the extent of CAD was defined as number of (1) coronary segments with plaque, or (2) major coronary arteries with plaque detected by MDCT as assessed by two independent observers. The clinical outcome (ACS) was adjudicated by a review committee using established AHA criteria; subjects with history of CAD (stent placement, bypass) were excluded. Results : Among 368 patients with acute chest pain (mean age 53±12 years, 61% male) 31 patients were determined to have ACS (8%). None of the 183 subjects without plaque (50%) had an ACS. Among the remaining 185 subjects (mean age 58.0±11.5 years, 68% male) in whom coronary plaque was detected, patients with ACS had a significantly more plaque (7.2±3.7 vs. 4.2±3.4, p&lt;0.0001 segments) as compared to subjects without ACS. Similar results were seen for calcified plaque and non-calcified plaque (6.5±3.7 vs. 3.6±3.5 segments, p&lt;0.0001; and 3.6±3.2 vs. 1.8±2.2 segments, p&lt;0.0001, respectively). In addition, the rate of ACS increased with the number of major coronary arteries with plaque (1-vessel: 6.8%, 2-vessels: 10.6%, 3 vessels: 30.8%, and 4-vessels: 25%; p&lt;0.01). In contrast, the ratio of non-calcified to calcified plaque was not different between patients with and without ACS (0.68±0.6 vs. 0.54±0.72, p=0.31). Conclusions: The extent of coronary plaque differs between subjects with and without ACS among patients presenting with acute chest pain. Detailed assessment of the extent and composition of coronary plaque may be helpful to assess risk of ACS among patients with acute chest pain but inconclusive initial ED evaluation.

Insertion/Deletion Polymorphism of the Angiotensin-Converting Enzyme (ACE) Gene in Coronary Artery Disease in an Iranian Population

Background: Because there are differences in frequency of insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene among different ethnic groups, we propose to evaluate the possible association with coronary heart disease in an Iranian population. Methods: We compared the ACE genotype distribution and derived allele frequency in 85 Iranian patients, who were hospitalized with coronary artery disease, with the genotype distribution and allele frequency in 88 healthy individuals, who were kidney donors. We also explored associations in the patients between the ACE insertion/deletion polymorphism and a history of myocardial infarction and coronary artery disease severity assessed by the number of major coronary arteries. Results: The D allele carriers genotypes (ID + DD) were more frequent in patients with coronary artery disease (CAD) (83%) compared with the control group (62.5%) (P = 0.000, odds ratio [OR] = 3.04), and the D allele frequency was significantly higher in patients with CAD (62%) that in control subjects (48%) (P = 0.008, OR = 1.78). Also, we found that frequencies of the D allele carrier genotypes (ID + DD) and the D allele were significantly higher in males with CAD compared with healthy males (P = 0.001 and P = 0.003, respectively), but there were no significant differences in females. There was also a significant excess of the D allele carriers genotypes and the D allele among patients with a history of myocardial infarction (P = 0.000 and P = 0.01, respectively). We found no association between the ACE gene polymorphism and the number of significant stenosed coronary arteries. Conclusions: The D allele and D allele carrier genotypes (ID + DD) are significant predictors for coronary artery disease in Iranian men (but not in Iranian women, and are significant predictors for myocardial infarction, but are not a marker for angiographically assessed coronary artery disease severity.

Polymorphism of angiotensin converting enzyme in Han populations and its relevance to the severity of coronary atherosclerosis

To explore the polymorphism angiotensin converting enzyme (ACE) in Han populations and its relevance to the severity of coronary atherosclerosis. The ACE genotype distribution was detected in 169 patients [aged (62.0 +/-9.9) years] with coronary artery disease (CAD) confirmed with angiography and in 168 normal controls [aged (61.0 +/-7.7) years]. The severity of coronary lesions in the patients was assessed by the number of major coronary arteries with more than 50% luminal obstructions and by the Gensini coronary score. Associations of the severity of coronary artery lesions with the ACE I/D polymorphism in the patients were analyzed. The frequencies of the ACE genotype in the CAD patients were 0.296 for DD, 0.391 for ID, and 0.314 for II genotypes, while in the normal controls the genotype distribution was in Hardy-Weinberg equilibrium (DD, 0.161; ID, 0.512; II, 0.327); a significantly excess of the DD genotype in CAD patients was found (P<0.01). No associations were observed between the ACE polymorphism and the number of significantly stenosed coronary arteries. The ACE gene polymorphism is a significant predictor for CAD in the Han population but is not a marker for the severity of coronary atherosclerosis.

Chlamydia pneumoniae IgG and the severity of coronary atherosclerosis

Background The aim of this study was to compare Chlamydia pneumoniae IgG and the extent of coronary atherosclerosis. Methods We investigated 92 patients with stable angina pectoris who underwent coronary angiography to assess chest pain. Before angiography, C. pneumoniae IgG was analyzed. The number of major coronary arteries (1–3) having at least one diameter narrowing (≥50%) stenosis was determined. The patients were divided into two groups of equal size, according to C. pneumoniae IgG levels. One group included individuals with C. pneumoniae IgG levels exceeding 46 enzyme-immuno-units (EIU)/L and the other consisted of subjects with IgG concentrations below 46 EIU/L. Results Subjects with higher antibody concentrations had a more severe disease. The number of diseased arteries was 2.1±0.8 (S.D.) and 1.4±0.6 (S.D.) for the two groups, respectively. The difference is highly significant ( p<0.0001). Conclusions This study suggests a causative relationship between C. pneumoniae IgG and the degree of coronary atherosclerosis. It does not, however, prove causality.

Demographic characteristics of the population undergoing cine coronary angiography at the Instituto do Coração of the Medical School of USP from 1986 to 1995.

To obtain information about the profile and behavior of a population with ischemic heart disease undergoing cine coronary angiography and to determine disease severity. Retrospective study assessing patients hospitalized at InCor from 1986 to 1995, in which the variables age, sex, and number of major coronary arteries with obstruction degree > or =40% were analyzed. We studied 18,221 patients and observed a significant increase in the number of females (22.8% to 25.2%, P=0.001) and an increase in age (57.1 +/- 29.3 to 60.4 +/- 10.7 years, P=0.0001). A significant increase in the incidence of multivessel disease was observed, which was more frequent among males (69.2% and 64.5%) and among the older patients (59.8 +/- 9.8 and 56.8 +/- 10.7 years, P=0.0001). A reduction in the incidence of single-vessel disease was also observed (66.2% vs 69.2% and 33.8% vs 30.5%, respectively, P<0.0001). A change in the profile of the population studied was observed as follows: patients undergoing cine coronary angiography at InCor were older, had a greater number of impaired major coronary arteries, and the number of females affected increased, leading to indices suggestive of a poorer prognosis.

Association of plasma homocysteine with the number of major coronary arteries severely narrowed

Association of plasma homocysteine with the number of major coronary arteries severely narrowed

ACC/AHA guidelines for coronary artery bypass graft surgery: executive summary and recommendations : A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to revise the 1991 guidelines for coronary artery bypass graft surgery).

The American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guidelines was formed to make recommendations regarding the appropriate use of diagnostic tests and therapies for patients with known or suspected cardiovascular disease. Coronary artery bypass graft (CABG) surgery is among the most common operations performed in the world and accounts for more resources expended in cardiovascular medicine than any other single procedure. Since the original Guidelines were published in 1991, there has been considerable evolution in the surgical approach to coronary disease, and at the same time there have been advances in preventive, medical, and percutaneous catheter approaches to therapy. These revised guidelines are based on a computerized search of the English literature since 1989, a manual search of final articles, and expert opinion. As with other ACC/AHA guidelines, this document uses ACC/AHA classifications I, II, and III as summarized below: Class I: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effective. Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness or efficacy of a procedure. Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy. Class IIb: Usefulness/efficacy is less well established by evidence/opinion. Class III: Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmful. ### A. Hospital Outcomes Seven core variables (priority of operation, age, prior heart surgery, sex, left ventricular [LV] ejection fraction [EF], percent stenosis of the left main coronary artery, and number of major coronary arteries with significant stenoses) are the most consistent predictors of mortality after coronary artery surgery. The greatest risk is correlated with the urgency of operation, advanced age, and 1 or more prior coronary bypass surgeries. Additional variables that are related …

Serum lipids, lipoprotein(a) and apo(a) isoforms in patients with established coronary artery disease and their relation to disease and prognosis after coronary by-pass surgery

Consecutive patients ( n=964) undergoing coronary angiography were studied and compared with a random population sample regarding serum lipids and lipoproteins with focus on lipoprotein(a) (Lp(a)) levels and apo(a) isoforms. The patients were also followed for 5 years after the angiography, and the progostic value of serum lipoproteins were analyzed. The patients were divided in two groups: Group 1 ( n=814) consisted of patients with angina pectoris and at least one coronary artery with 50% stenosis and group 2 ( n=150) patients with none of the coronary arteries significantly obstructed (<50%). As controls a random population sample was selected ( n=197). Blood samples were collected before coronary angiography for determination of serum lipids, Lp(a) and isoforms of apo(a). When group 1 and group 2 patients were compared, group 1 was found to have higher serum cholesterol, triglycerides, apoB and Lp(a) as well as lower HDL and apoAI. When group 1 was compared with the random sample, after correction for age and sex, similar differences were observed, except that the difference in Lp(a) was not significant. The high Lp(a) levels among patients was found to be primarily due to the female patients, where the difference compared to both group 2 and controls was highly significant ( P=0.007 and P=0.001, respectively). There was a significant difference in the apo(a) isoform distribution between group 1 patients and control subjects ( P=0.0003), with a higher frequency of low molecular weight isoforms among patients. This was also significant for the male subgroup ( P=0.001). Lp(a), LDL, total cholesterol, triglycerides, apoB, HDL and apoAI were significantly related to the number of major coronary arteries with >50% stenosis. Mortality during follow-up was,in a univariate analysis, significantly correlated to several factors related to the degree of heart disease and to LDL ( P=0.02) and apoB ( P<0.01). Increased mortality was, however, related to low levels of apoB and LDL. For cardiac mortality no significant correlation to lipoprotein variables were found. In conclusion established lipoprotein risk factors were more frequent among patient with angina pectoris and verified coronary stenosis. Furthermore high Lp(a) levels and a high frequency of low molecular weight isoforms of apo(a) were found in coronary patients. Higher Lp(a) levels were observed both for female and male patients, the differences were, however, significant only for the female patients. None of the lipoprotein variables could predict coronary death during the follow-up period.

Circulating transforming growth factor beta 1 and coronary artery disease.

Transforming growth factor beta 1 (TGF-beta 1), a multifunctional cytokine, is involved in many physiological and pathological processes and possibly in atherogenesis. We explored the association between circulating plasma TGF-beta 1 measured by ELISA and coronary artery disease (CAD) assessed angiographically in 371 Caucasian patients (269 men and 102 women) aged < or = 65 years. While mean +/- s.e.m total TGF-beta 1 was not different among patients with (56.9 +/- 1.5 ng/ml) or without (54.6 +/- 2.8 ng/ml) angiographically demonstrable CAD, naturally active TGF-beta 1 was significantly higher in CAD patients (1.74 +/- 0.18 vs 0.96 +/- 0.17 ng/ml, P < 0.01). Active TGF-beta 1 increased with the number of major coronary arteries with more than 50% luminal obstruction (P < 0.01) and patients with triple vessel disease had twice the level of those with no or mild vessel disease (2.15 +/- 0.46 vs 1.12 +/- 0.14 ng/ml, P < 0.001). We found no relationship between TGF-beta 1 and Lp(a), but TGF-beta 1 was significantly correlated with circulating fibrinogen (r = 0.178, P = 0.005) and fasting glucose (r = 0.177, P = 0.007) levels. Our study identifies an increase in active TGF-beta 1 levels with both the occurrence and severity of CAD which is independent of standard CAD risk factors. This may reflect a 'double-edged sword' effect of TGF-beta 1 in that it may reduce atherogenesis by inhibiting smooth muscle cell proliferation but, when there is ongoing vessel wall injury, enhance it by promoting excessive extracellular matrix accumulation. The outcome could represent a complex balance between these two competing influences.

Genotype distribution of angiotensin-converting enzyme polymorphism in Australian healthy and coronary populations and relevance to myocardial infarction and coronary artery disease.

Angiotensin-converting enzyme is a key component of the renin-angiotensin system that plays an important role in cardiovascular regulation. An association between the angiotensin-converting enzyme insertion/deletion (I/D) polymorphism and increased coronary risk has been found in some studies but not in others. To explore this further in an Australian white population, we compared the ACE genotype distribution in 550 patients aged 37 to 65 years with coronary artery disease documented by angiography with the genotype distribution in 404 healthy school children aged 6 to 13 years. We also explored associations in the patients between the angiotensin-converting enzyme I/D polymorphism and a history of myocardial infarction and coronary artery disease severity assessed by the number of major coronary arteries with more than 50% luminal obstructions and by the Green Lane coronary score. The frequencies of the angiotensin-converting enzyme genotype in the coronary artery disease patients were 0.236 for I/I, 0.395 for I/D, and 0.369 for D/D genotypes. This distribution with an excess of the D/D genotype was significantly different (chi 2 = 23.69, P < .0001) from that in the school children, in whom the genotype distribution was in Hardy-Weinberg equilibrium (I/I, 0.21; I/D, 0.54; D/D, 0.25). There was also a significant excess of D/D genotype among patients with a history of myocardial infarction (chi 2 = 9.42, P = .009), and there was the same D/D excess in the subgroup of children (n = 60) with two or more grandparents who had had coronary artery disease. We found no associations between the angiotensin-converting enzyme polymorphism and the number of significantly stenosed coronary arteries (chi 2 = 2.069, P = .91). We conclude that the D/D genotype is a significant predictor for coronary artery disease events in the Australian white population but is not a marker for angiographically assessed coronary artery disease severity. The angiotensin-converting enzyme genotype-associated increased risk for coronary events may be mediated more by angiotensin II-induced coronary vasoconstriction than by an increase in injury-related smooth muscle cell proliferation in the coronary vasculature.

Long-term prognostic significance of M mode echocardiography in young men after myocardial infarction.

To evaluate the power of measurements of left ventricular size and function for predicting long term (82 month) mortality by performing echocardiography in 97 men who had survived an acute myocardial infarction. University hospital specialising in cardiology. 97 consecutive male patients who had survived a myocardial infarction. The additive prognostic value of functional measurements to that provided by primary risk factors (smoking habits and lipoprotein levels), radiological heart size, exercise capacity, and number of major coronary arteries with haemodynamically significant stenoses was evaluated. An echo index was calculated from three echocardiographic variables (yielding one score point each if: left ventricular diameter at the end of diastole (LVDD) > or = 5.7 cm, left ventricular fractional shortening < or = 24%, and E point-separation (EPSS) > or = 10 mm). 17 cardiac deaths occurred during follow up. Univariate analysis showed that treatment with loop diuretics for heart failure (P < 0.01), LVDD (P < 0.01), left ventricular diameter at the end of systole (LVDS) (P < 0.001), left atrial diameter (P < 0.001), fractional shortening (P < 0.05), and echo index (P < 0.001) were all associated with cardiac death. Angiographically determined regional wall motion disturbances (P < 0.005) and angiographic ejection fraction (P < 0.001) were also associated with cardiac death, as was the number of major coronary arteries with significant stenosis (P < 0.05). When all significant echocardiographic variables from univariate analysis were entered into Cox proportional hazards survival analysis, LVDS and left atrial diameter contributed independently to the prediction of cardiac death. If angiographic data were also entered into the model, the echo index made an independent contribution to the prediction of cardiac death. Among young male patients with a previous myocardial infarction, a simple M mode echocardiographic examination can identify high and low risk patients and improve the prediction of cardiac death made from clinical information, exercise test, chest x ray and angiographically determined ejection fraction.

冠動脈硬化を有する患者における大動脈脈波速度 冠動脈撮影所見との対比

This study was conducted to investigate the relationship between aortic pulse wave velocity (PWV) and coronary atherosclerosis. We measured PWV in 105 subjects (84 males and 21 females; age 59 +/- 0.5) who received coronary angiographic examination (CAG). PWV was measured by simultaneous recording of pulse waves from the left carotid and the left femoral arteries, electrocardiogram and phonocardiogram. The subjects were classified into 4 groups according to the number of major coronary arteries having stenosis, that is, N group with normal CAG, 1 vessel disease (VD) group, 2VD group and 3VD group. The PWV value was significantly greater only in 3VD group (n = 10, age 63 +/- 3.6, PWV 10.0 +/- 0.88 m/sec) than that in N group (n = 18, age 53 +/- 2.0, PWV 8.0 +/- 0.34 m/sec). No significant difference was observed between PWV value in N group and that in all patients with coronary artery stenosis (n = 87, age 60 +/- 2.0, PWV 8.9 +/- 0.2 m/sec). To further investigate the relationship between PWV values and CAG findings, we used a CAG score which means the sum of the points assigned to each coronary artery segment (American Heart Association) according to the severity of stenosis (0, 1, 2, 3, and 4 for normal, less than 49% stenosis, 50 to 74% stenosis, 75 to 99% stenosis, and complete occlusion, respectively). The PWV values significantly correlated with the CAG score and also with age by a simple regression analysis. Multivariate analysis, however, revealed that PWV values did no longer correlate with CAG score. PWV values still significantly correlated with age.(ABSTRACT TRUNCATED AT 250 WORDS)

Sudden coronary death: Comparison of patients with to those without coronary thrombus at necropsy

Among 70 victims of sudden coronary death (SCD), certain clinical and morphologic findings in the 13 with a coronary thrombus are compared with the findings in 57 victims without a coronary thrombus. The 13 with a thrombus were younger than those without (mean age 43 vs 51 years, p less than 0.02); had a lower mean percent of cross-sectional area (XSA) narrowing by plaque at the site of maximal coronary stenosis (89% vs 95%, p less than 0.01); and had a higher mean percent of 5-mm segments of the 4 major epicardial coronary arteries minimally narrowed (0 to 25% in XSA) by plaque (27% vs 19%, p less than 0.001). No differences occurred in the 2 groups with regard to sex, previous angina pectoris or clinical acute myocardial infarction, healed myocardial infarction at necropsy, mean heart weight, number of major coronary arteries narrowed 76 to 100% in XSA by atherosclerotic plaque, or the mean percent of 5-mm segments of the 4 major epicardial coronary arteries narrowed 76 to 100% in XSA by atherosclerotic plaque. Thus, coronary thrombi are infrequent in victims of SCD, and when observed, their significance is uncertain because victims of SCD without coronary thrombi have similar amounts of severe coronary narrowing.

Left ventricular hemodynamics in patients with coronary artery disease and in normal subjects: Correlations with the extent of coronary artery lesions and the electrocardiogram

Left ventricular hemodynamics were studied during supine leg exercise immediately prior to coronary arteriography in seventy-one patients with coronary artery disease and nineteen without evidence of heart disease. Patients were divided into six groups, based on the number of major coronary arteries (right coronary, left anterior descending, left anterior descending diagonal, left circumflex, left circumflex marginal) with greater than 75 per cent obstruction. Mean resting and exercise left ventricular end-diastolic pressure (LVEDP) and increase in LVEDP during supine exercise rose progressively with more extensive coronary artery disease. All patients without coronary artery disease or with disease confined to one coronary artery had LVEDP of less than 24 mm Hg during exercise. There was no significant difference between groups with coronary artery disease in regard to stroke volume, heart rate and systemic arterial pressure. There was no significant difference in LVEDP at rest or during exercise between patients with normal and those with abnormal resting electrocardiograms. However, in patients with abnormal electrocardiograms after exercise, the mean LVEDP was significantly higher than in those with normal electrocardiograms after exercise (P < 0.05). Other hemodynamic differences between patients with normal and those with abnormal electrocardiograms after exercise were insignificant. The degree of rise in LVEDP with supine leg exercise in patients who have coronary artery disease is in part related to the number of coronary arteries with severe obstruction, and an abnormal electrocardiogram after exercise is associated with a high LVEDP during exercise.