Acute myocardial infarction with normal coronary arteries is a well known condition, which is typically diagnosed in young patients. Coronary vasospasm, inherited, acquired or malignancy-induced hypercoagulable state, collagen vascular disease and coronary arterial embolism have been considered as underlying etiologic factors. An association between migraine with aura and increased risk of ischemic stroke, angina and myocardial infarction has been demonstrated in studies. Patients with migraine and especially with aura should be followed closely against cardiovascular events even if they are young and do not have traditional risk factors.

The study aims to evaluate sex differences in extent and severity of coronary artery disease (CAD) and myocardial findings at autopsy among young people with fatal ischemic heart disease (IHD).

Women with acute coronary syndrome are less likely than men to display obstructive CAD at angiography. This suggests unique mechanisms of acute coronary syndrome exist in women or may reflect prehospital death of women with the most severe CAD.

Reports of autopsies by the Office of the Chief Medical Examiner of New York City on people aged 21 to 54 years who died between January 1, 2006, and December 31, 2008, were reviewed. A total of 639 cases of death due to atherosclerotic or arteriosclerotic cardiovascular disease according to the medical examiner were analyzed. Significant CAD was defined as ≥75% cross-sectional area stenosis in an epicardial vessel or ≥50% left main.

Women were less likely to have obstructive CAD (63% vs 77% of men, P = .002). There was pathologic evidence of myocardial infarction (MI) in 43% of cases, 17% of which had nonobstructive CAD. Frequency of MI did not vary by sex overall (38% of women vs 45% of men, P = .18) or among those without significant CAD (23% vs 29%, P = .45).

Among young people determined at autopsy to have died of IHD, fewer women had obstructive CAD, consistent with angiographic data in other IHD syndromes. Pathologic evidence of MI may exist in the absence of obstructive CAD.

There is a paucity of data concerning the clinical outcome of patients presenting with acute myocardial infarction (AMI) and near-normal coronary angiograms. The purpose of this study was to evaluate the clinical outcome and the prognosis of the patients with near-normal coronary angiograms who were registered in the Korean Acute Myocardial Infarction Registry (KAMIR).

The subjects were divided into three groups according to findings from coronary angiograms performed between September 2005 and November 2006. Among 8510 consecutive AMI patients, 372 patients (Group I) had near-normal coronary arteries, 6136 patients (Group II) had one- or two-vessel disease, and 2002 patients (Group III) had three-vessel or left main disease.

Clinical characteristics, in-hospital mortality, and major cardiac adverse events (MACE) were analyzed. Group I was younger, had the lower prevalence of DM, and showed the higher percentage of previous angina history compared to the other two groups. Group III showed a higher incidence of in-hospital mortality, but there was no significant difference between Group I and Group II (2.6% in Group II and 2.2% in Group I, p=0.952). Furthermore, MACE at 1 month, 6 months and 12 months revealed no significant difference between Groups I and II (12 month MACE: 7.8% in Group I and 12.2% in Group II, p=0.359).

Patients with near-normal coronary angiograms had similar clinical outcomes and prognosis compared with one- or two-vessel diseased patients presenting with an acute myocardial infarction.

We sought to compare clinical profiles and midterm prognosis of patients with normal coronary arteries presenting with ST-elevation ACS (STE-ACS) versus non-ST-elevation ACS (nSTE-ACS).

There are limited data regarding ACS in patients with normal coronary arteries, and especially clinical differences between ST-ACS and nSTE-ACS patients have not been evaluated sufficiently.

The study group comprised 190 patients (mean age: 53.2 years, 63.1% males, 63.6% STE-ACS) presenting with ACS and normal coronary angiograms. The participants were evaluated in terms of 42 clinical variables. MACE [cardiac death (CD) and hospitalization for angina (HA)] were the study end points.

STE-ACS in comparison to nSTE-ACS patients were younger (P < 0.01), were more frequently males (P < 0.01), had more often infection prior to ACS (P < 0.01), higher hsCRP on admission (P < 0.01), and greater infarct size, measured by maximal troponin I (P < 0.01). By multivariate analysis in this subgroup, predictors of outcome were hsCRP (P = 0.03) and raised troponin I (P = 0.02). nSTE-ACS in comparison to STE-ACS patients were more obese (BMI, P < 0.01), had higher LDL cholesterol (P < 0.01), fasting glucose (P = 0.03). LDL cholesterol (P = 0.02) and fasting glucose (P = 0.03) emerged as independent predictors of outcome in these patients. Mean follow-up period was 25.4 months. STE-ACS patients had twice fewer MACE rate than nSTE-ACS patients [(1-CD, 12-HA; 11%) vs (1-CD, 16-HA; 25%), respectively, log rank P < 0.01].

STE-ACS and nSTE-ACS patients with normal coronary arteriography have different clinical profiles. In nSTE-ACS patients more pronounced metabolic abnormalities were identified, while in STE-ACS patients inflammatory background was more significant.

The purpose of this study was to evaluate the incidence of peripartum myocardial ischemia in Canada.

We identified the cohort of women who were admitted to Canadian hospitals for delivery between 1970 and 1998 to calculate the incidence rate and to evaluate potential risk factors.

One hundred fourteen of 10,032,375 women delivered in Canadian hospitals between 1970 and 1998 had peripartum myocardial ischemia recorded as a discharge diagnosis. The overall crude incidence rate was 1.1 (95% confidence interval 0.93, 1.37) women with peripartum myocardial ischemia per 100,000 women delivering per year as noted in the Canadian Hospital Morbidity database. Rates did not increase over time but increased with maternal age. Identified risk factors were diabetes mellitus, hyperlipidemia, and chronic heart disease. The case fatality rate among women with the disease was 1.8%.

The incidence of peripartum myocardial ischemia did not increase between 1970 and 1998 in Canada, despite an aging cohort with more prevalent medical comorbidities. Maternal mortality from this event is lower than previously described.

We evaluated migraine as an independent risk factor for subsequent coronary heart disease (CHD) events among women in the Women's Health Study (WHS) and men in the Physicians' Health Study (PHS).

Although several studies have suggested that migraine is associated with increased risk of stroke, there are few and conflicting data on whether migraine predicts risk of future CHD events.

The WHS is an ongoing randomized, double-blind, placebo-controlled trial of low-dose aspirin and vitamin E in the primary prevention of cardiovascular disease and cancer in 39876 women health professionals aged > or =45 years in 1993, and the PHS is a completed randomized, double-blind, placebo-controlled trial of aspirin and beta-carotene in the primary prevention of cardiovascular disease and cancer in 22071 men physicians aged 40 to 84 years in 1982. Primary endpoints were defined as major CHD (nonfatal myocardial infarction [MI] or fatal CHD) and total CHD (major CHD plus angina and coronary revascularization).

After adjusting for other CHD risk factors, female health professionals and male physicians reporting migraine were not at increased risk for subsequent major CHD (women: relative risk [RR], 0.83; 95% confidence interval [CI], 0.53 to 1.29; men: RR, 1.02; 95% Cl, 0.79 to 1.31) or total CHD (women: RR, 1.01; 95% Cl, 0.76 to 1.34; men: RR, 0.98; 95% Cl, 0.82 to 1.18). When considered separately, there was also no increase in risk of MI or angina.

These prospective data suggest that migraine is not associated with increased risk of subsequent CHD events in women or men.

Sex hormones exert important effects on the vasculature. Female sex hormones have been reported to enhance endothelial function, reduce oxidative stress, and protect against atherosclerosis. However, the effects of estrogen on vascular compliance have not been studied. Recently, noninvasive instrumentation that estimates vascular compliance by recording the radial artery pulse contour has been introduced. Reductions in the oscillatory or reflected component of the diastolic waveform have been observed in various clinical conditions, including hypertension, diabetes mellitus, and congestive heart failure, and may reflect endothelial dysfunction at the site of resistance vessels. In this study the authors examined gender-related vascular compliance in a cohort of young, healthy, predominantly nonsmoking, medication-free men and women to determine the influence of cardiovascular risk factors, including family and social history, serum lipids, plasma homocysteine, and insulin levels on vascular compliance.

The volunteers, consisting of 151 healthy men and women (mean age 24A+/-4 years) completed a questionnaire detailing family and social history, medication use, and exercise habits. Large (C1) and small (C2) vessel compliance and various cardiovascular parameters were derived from arterial pulse wave contour analysis. Systolic, diastolic, and mean arterial blood pressure, pulse pressure, and pulse rate were determined simultaneously by oscillometry. Blood for fasting serum lipids, plasma homocysteine, and serum insulin were obtained in a subset of 135 subjects.

The questionnaire revealed that 38% of parents had a history of hypertension, 31% had dyslipidemia, and 15% had coronary heart disease. C2 was lower in subjects with parental dyslipidemia. Compared to men, women had lower C2; lower systolic blood pressure, mean arterial pressure, and pulse pressure; higher serum high-density lipoprotein cholesterol; lower serum triglycerides; and lower plasma homocysteine, but similar serum insulin levels. C1 correlated with height and pulse pressure, whereas C2 was proportional to height and weight and inversely related to systemic vascular resistance. Multivariate regression analysis showed that stroke volume, total vascular impedance, cardiac output, female gender, and systemic vascular resistance independently predicted changes in C2, but that height was not a significant factor.

Women have reduced C2 despite lower systolic blood pressure and pulse pressure and more favorable lipid and homocysteine levels. C2 is independent of height and is lower in subjects with parental dyslipidemia. These data indicate that female sex hormones have unexpected negative effects on small vessel compliance. They may help to explain why premenopausal women hospitalized for myocardial infarction have higher mortality rates than men of the same age.

Despite being an unprecedented departure from normal physiology, the combined oral contraceptive is not only highly effective, but it also has a remarkably good safety record. Concerns over safety persist, though, particularly with regard to venous thromboembolism (VTE), stroke and myocardial infarction (MI). Epidemiological studies consistently show an increase in risk of VTE, but the results are more contentious with regard to arterial diseases. Despite 40 years of research, the mechanisms behind these adverse effects are not understood. In this review, we integrate information from published studies of the epidemiology and pathology of the occlusive vascular diseases and their risk factors to identify likely explanations for pathogenesis in oral contraceptive users. Oral contraceptives induce both prothrombotic and fibrinolytic changes in haemostatic factors and an imbalance in haemostasis is likely to be important in oral contraceptive-induced VTE. The complexity of the changes involved and the difficulty of ascribing clinical significance has meant that uncertainty persists. A seriously under-researched area concerns vascular changes in oral contraceptive users. Histologically, endothelial and intimal proliferation have been identified in women exposed to high plasma estrogen concentrations and these lesions are associated with thrombotic occlusion. Other structural changes may result in increased vascular permeability, loss of vascular tone and venous stasis. With regard to arterial disease risk, epidemiological information relating to dose effects and joint effects with other risk factors, and studies of pathology and changes in risk factors, suggests that oral contraceptive use per se does not cause arterial disease. It can, nevertheless, synergise very powerfully with subclinical endothelial damage to promote arterial occlusion. Accordingly, the prothrombotic effects of the oral contraceptive estrogen intervene in a cycle of endothelial damage and repair which would otherwise remain clinically silent or would ultimately progress - in, for example, the presence of cigarette smoking or hypertension - to atherosclerosis. Future work in this area should focus on modification of the effects of established risk factors by oral contraceptive use rather than modification of the supposed risk of oral contraceptive use by established risk factors. Attempts to understand vascular occlusion in oral contraceptive users in terms of the general features of VTE or with reference to atherosclerosis may be limiting, and future work needs to acknowledge that such occlusions may have unique features. Unequivocal identification of the mechanisms involved would contribute considerably to the alleviation of fears over vascular disease and to the development of even safer formulations.

There is conflicting information about whether short-term mortality after myocardial infarction is higher among women than among men after adjustment for age and other prognostic factors. We hypothesized that younger, but not older, women have higher mortality rates during hospitalization than their male peers.

We analyzed data on 384,878 patients (155,565 women and 229,313 men) who were 30 to 89 years of age and who had been enrolled in the National Registry of Myocardial Infarction 2 between June 1994 and January 1998. Patients who had been transferred from or to other hospitals were excluded.

The overall mortality rate during hospitalization was 16.7 percent among the women and 11.5 percent among the men. Sex-based differences in the rates varied according to age. Among patients less than 50 years of age, the mortality rate for the women was more than twice that for the men. The difference in the rates decreased with increasing age and was no longer significant after the age of 74 (P< 0.001 for the interaction between sex and age). Logistic-regression analysis showed that the odds of death were 11.1 percent greater for women than for men with every five-year decrease in age (95 percent confidence interval, 10.1 to 12.1 percent). Differences in medical history, the clinical severity of the infarction, and early management accounted for only about one third of the difference in the risk. After adjustment for these factors, women still had a higher risk of death for every five years of decreasing age (increase in the odds of death, 7.0 percent; 95 percent confidence interval, 5.9 to 8.1 percent).

After myocardial infarction, younger women, but not older women, have higher rates of death during hospitalization than men of the same age. The younger the age of the patients, the higher the risk of death among women relative to men. Younger women with myocardial infarction represent a high-risk group deserving of special study.

This is an observational study in which we compared the clinical characteristics and the long-term course of young patients having acute myocardial infarction and angiographically normal coronary arteries and young patients showing significant coronary artery disease. In 87 patients aged < or = 40 years who suffered an acute myocardial infarction, enrolled in a prospective study over a period of 6.5 years, coronary anatomy was determined by angiography within a month of admission. The risk factors, clinical data, ventricular function and the long-term outcome were compared between patients with normal angiograms (Group 1, n = 12) and patients with coronary artery disease (Group 2, n = 75). Patients in Group 1 had a lower number of risk factors associated with them (17% vs. 64% with > 1 risk factor, P < 0.005), were younger (32 +/- 5 vs. 36 +/- 4, P < 0.01), lighter smokers (25% vs. 55% for > or = 2 packs per day, P < 0.05), had less frequent hypertension (0 vs. 25%, P < 0.05), hypercholesterolemia (17% vs. 52%, P = 0.02) and had a lower mean total cholesterol level (201 +/- 42 vs. 245 +/- 60 mg/100 ml, P < 0.05) than patients in Group 2. They also had a more common onset of their infarction during heavy physical exertion (67% vs. 17%, P < 0.001). A history of previous myocardial infarction, infarct location, global left ventricular function and regional wall motion were similar in both groups. After a mean follow-up period of 41 +/- 23 months, no patient died or had a second myocardial infarction in Group 1, and 4 patients had died in Group 2. The appearance of angina, less frequent in Group 1 than Group 2, tended to correlate with the extension of the coronary artery disease. We concluded that young patients with myocardial infarction have good prognosis irrespective of the coronary anatomy, although patients with normal coronary angiograms had less risk factors and less frequent new ischaemic events.

1. To study the effect of acute nitric oxide (NO) inhibition on the rat heart both in vitro and in vivo, male Wistar rats received a single bolus injection of saline, N omega-nitro-L-arginine methyl ester (L-NAME; 0.5, 1.5, 5.0, 15.0 and 45.0 mg/kg) and D-NAME (45.0 mg/kg). 2. Animals were killed 72 h after the bolus injection of L-NAME and the hearts were removed and studied under light microscopy. In other groups of animals; saline, L-NAME and D-NAME were administered as above and the mean arterial blood pressure (MABP/carotid) was recorded. Furthermore, L-NAME was also administered in the drinking water (20 mg/kg per day) for 72 h and animals were then killed and their hearts evaluated as described above. Hearts of control animals were perfused in vitro and coronary flow was measured following saline, L-NAME (45 micrograms/heart) and D-NAME (45 micrograms/heart). 3. Areas of necrosis were observed in the left ventricle of animals that had received L-NAME at 5.0, 15.0 and 45.0 mg/kg. Also, only doses higher than 1.5 mg/kg caused an important increase in MABP. The frequency and extent of the lesions paralleled the dose of L-NAME administered and no lesions were observed in D-NAME- and saline-treated animals. 4. The oral administration of L-NAME also caused myocardial lesions similar to those described above, but the frequency and extent of these lesions were more discrete compared with those observed following 5.0 mg/kg, i.v., L-NAME. 5. Bolus injection of L-NAME into control rat hearts in vitro resulted in a small and transient fall in coronary flow (17.2 +/- 1.4 and 12.2 +/- 1.2 mL/min before and after L-NAME administration, respectively) within 30 s and this was followed 4.5 min later by a further (11.5 +/- 1.6 mL/min) decrease. The administration of D-NAME to control hearts caused no change in coronary flow. 6. In conclusion, the acute inhibition of NO biosynthesis by L-NAME causes myocardial necrosis. Both high levels of MABP and a small but significant reduction in coronary flow (associated or not) can be responsible for the lesions we found.

To determine the prevalence rate and clinical and hemodynamic profile of patients with myocardial infarction (MI) with angiographically normal coronary arteries, we analyzed 3,403 consecutive angiograms performed within a 4.5-year period. Of these studies, 1,124 were performed following an acute MI. Through a computerized search, 12 patients were identified who had documented MI with normal or insignificant (< 30% stenosis in one epicardial vessel only) coronary disease. Q-wave MI developed in five patients (group A) and non-Q-wave MI developed in seven patients (group B). Group A patients were all men whereas group B patients were all women. Overall, group A patients were younger (p = 0.003), had a longer smoking history (p = 0.008), and a higher cardiac index (p = 0.005). In ten patients, areas of localized dyskinesia or hypokinesia were shown on left ventricular cineangiography. Mitral valve prolapse was present in four of the patients and varying degrees of mitral regurgitation were identified in another six. The prevalence rate of MI with angiographically normal coronary arteries was 1% in this study. This entity had a bimodal age and sex distribution: a younger age group, all men, with a stronger cigarette smoking history who had Q-wave MI vs an older age group, all women, and no significant association with cigarette smoking who developed non-Q-wave MI. A mean follow-up of 4 years demonstrated a favorable prognosis in both groups.

The relations between triglyceride-rich lipoproteins, alimentary lipaemia and coronary heart disease (CHD) have remained obscure and much debated. We studied the basal and postprandial plasma levels of chylomicron remnants and very low density lipoproteins (VLDL) of varying particle size in 32 male postinfarction patients (mean (S.D.) age 48.8 (3.2) years) and in 10 age-matched control men. The selective quantification of postprandial intestinal and hepatic lipoproteins was accomplished by determining apolipoproteins B-48 and B-100 in lipoprotein subfractions of Svedberg flotation (Sf) rates > 12 before and 3, 6 and 12 h after an oral fat load. Since all patients had undergone two coronary angiographies with an intervening time interval of around 5 years, lipoprotein fractions were examined in relation to the global severity as well as the rate of progression of coronary lesions. The postprandial plasma levels of small chylomicron remnants (Sf 20-60 apolipoprotein B-48) were found to relate distinctly to the rate of progression of coronary lesions between the angiographies (r = 0.51, P = 0.01). Adjustment for the possible confounding effect of the HDL cholesterol and dense LDL apolipoprotein B concentrations did not substantially alter the strength of this association. Neither the increment of plasma triglyceride during the postprandial period nor the concentrations of other lipoprotein fractions closely reflected the amount of small chylomicron remnants in the circulation or correlated with progression of coronary lesions. Our data suggest that small chylomicron remnants are implicated in the progression of coronary artery disease.

Three patients below 21 years of age presented with typical symptoms, electrocardiographic pattern, and levels of enzymes suggestive for acute myocardial infarction. Various risk factors for coronary artery disease were present in all three patients. Coronary angiography showed normal coronary arteries in all. Thus, acute myocardial infarction may be experienced even in very young patients. Clinical and angiographic findings are discussed on the basis of the existing reports in the literature.

The incidence of minimal residual atherosclerotic coronary obstruction after successful intravenous thrombolytic therapy was evaluated in 799 patients with acute myocardial infarction. Minimal residual coronary obstruction (less than or equal to 50%) was observed on selective coronary angiography performed 90 min after initiation of thrombolytic therapy in 43 patients (5.5%). In 42 other patients (5.4%), a greater than 50% but less than 100% residual stenosis noted at 90 min demonstrated further resolution of obstruction to less than 50% at an angiographic follow-up study 7 to 10 days later. Patients with minimal residual coronary obstruction were significantly younger (52 +/- 10.7 versus 56.7 +/- 10 years; p = 0.002) and had less multivessel coronary disease (p less than 0.001), better initial left ventricular ejection fraction (54 +/- 12% versus 50.2 +/- 11.4%; p = 0.006) and a lower in-hospital mortality rate (1% versus 7%; p = 0.04) than did patients who had a significant (greater than 50%) residual coronary obstruction after intravenous thrombolysis. Long-term follow-up study of patients with a minimal coronary lesion (average 1.5 +/- 0.6 years) and those with significant residual stenosis (average 1.6 +/- 0.7 years) demonstrated that the incidence of death (2.4% in patients with minimal stenosis versus 3.5% in those with significant stenosis) and recurrent myocardial infarction (5% each) were similar in both groups. New strategies are needed to prevent coronary rethrombosis in patients with minimal atherosclerosis after thrombolytic therapy for acute myocardial infarction.

Thirty-six consecutive patients with evolving acute myocardial infarction underwent emergent coronary angiography and intracoronary thrombolysis with urokinase. Nineteen of the patients had had angina before the infarction (group A), whereas the infarction was unheralded in the remaining 17 (group B). Thirty-two vessels (88%) were patent at follow-up angiography performed after 3 to 4 weeks, and the residual stenosis was 87% +/- 14% in group A and 47% +/- 25% in group B (p less than 0.001). Coronary spasm was provoked by ergonovine maleate in four of 12 patients in group A (33%) and in three patients in group B (18%). Coronary revascularization was undertaken in nine patients in group A and three in group B. These results indicate that patients with angina preceding acute myocardial infarction are more likely to have significant stenosis even at the late follow-up stage and to have a more urgent need for subsequent coronary revascularization. It also seems apparent that thromboembolism in most patients and coronary spasm in a few patients without significant coronary narrowing play significant causal roles in the onset of acute myocardial infarction.

To determine the natural history of myocardial infarction (MI) in the absence of angiographically significant (no lesion greater than or equal to 50% diameter stenosis) fixed coronary artery disease (CAD), clinical and angiographic data and late outcome were studied in 43 such patients. The mean age was 45 +/- 11 years; 32 patients (74%) were cigarette smokers. Mild fixed CAD, present in 38 patients (88%), was more frequent in the artery supplying the MI zone (p less than 0.01). Filling defects or serial angiographic resolution of obstruction in the artery supplying the MI zone were present in 14 patients (33%). At late follow-up, 14 major cardiac events occurred in 9 patients, including revascularization in 3, recurrent MI in 6 and cardiac death in 5. Of 35 patients undergoing catheterization within 1 year of the index MI, cumulative risk of a major cardiac event was 9 +/- 4, 12 +/- 5 and 20 +/- 7% at 3, 19 and 37 months, respectively. Myocardial infarction in the absence of significant fixed CAD tends to occur in young smokers with mild CAD in the artery serving the MI zone. Superimposed intracoronary thrombus can be frequently implicated. In these patients, subsequent major cardiac events may occur more frequently than previously reported.

Myocardial infarction with normal coronary arteries was identified in 74 patients with a mean age of 43 years (range 19 to 66). A mean follow-up period of 10.5 years after documented myocardial infarction and 8.6 years after cardiac catheterization was obtained. The survival rate was 85% (n = 63). There were no statistical differences in age or clinical risk factor prevalence between survivors and nonsurvivors. Moderate (55%) to severe (27%) left ventricular impairment was more common in nonsurvivors. Nine of 11 deaths were cardiovascular, 6 were sudden and 8 occurred in patients with moderate to severe global left ventricular impairment. Seventy-six percent of survivors were asymptomatic and 86% were fully active at follow-up. Two survivors and three nonsurvivors experienced a second myocardial infarction. The clinical risk factors of the study group (Group I) were compared by age, sex and year of catheterization with risk factors in two matched groups. Group II consisted of 74 patients with coronary occlusive disease and myocardial infarction and Group III consisted of 148 patients with normal arteriograms. Group I differed from Group II in having fewer clinical risk factors (p = 0.01 to less than 0.0001). Cigarette smoking did not differ significantly between Group I (72%) and Group II (69%) but was less common in Group III (45%) (p less than 0.001). Hormone therapy or the peripartum state was more common in women in Group I (34%) than in women in Group III (14%) (p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial infarction is increasingly recognized as a complication of cocaine abuse. A significant number of persons suffering from myocardial infarction associated with cocaine abuse do not have significant coronary atherosclerosis, and the mechanism for infarction in these patients has remained obscure. This report describes a young man with angiographically normal coronary arteries in whom cocaine abuse produced coronary artery spasm leading to coronary thrombosis and infarction.

Coronary angiography was performed 3 to 6 months after myocardial infarction in 107 males below the age of 45 (mean age 39.7 +/- 3.9, range 23-44 years). The coronary angiograms were allocated to various groups according to the presence or absence of obvious atheromatous changes. Metabolic evaluation included determination of cholesterol and triglyceride concentrations in the major serum lipoproteins. Marked elevation of low density lipoprotein (LDL) cholesterol concentration was found in patients with angiographic evidence of atheromatosis, in contrast to patients with normal coronary angiograms or with single occlusion and no other abnormalities. Thus, there was a correlation between angiographic appearance of the coronary arteries and disturbances of LDL metabolism. It is proposed that coronary angiography may distinguish between atheromatous and non-atheromatous pathogenesis of myocardial infarction at young age.

The relationship of serum lipoprotein and apolipoprotein concentrations to angiographically determined coronary artery disease was investigated in 105 consecutive male survivors of myocardial infarction under the age of 45. Concentrations and composition of lipoproteins, lipid indexes, and nonlipid risk factors (tobacco consumption, hypertension, reduced glucose tolerance, and obesity) were related to a recently developed scoring system for semiquantitative estimation of diffuse coronary atheromatosis, as well as to the number and severity of significant coronary artery stenoses. The concentrations of cholesterol in very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL), in combination with serum triglyceride or VLDL triglyceride level, comprised the best set of independent discriminatory lipid variables between patients and control subjects. In the patients, LDL cholesterol and apolipoprotein B levels showed strong relationships to the extent and severity of coronary atheromatosis but not to the number and severity of distinct coronary stenoses. HDL2 cholesterol concentration correlated inversely with the coronary atheromatosis score, whereas other variables reflecting HDL concentration and composition or VLDL lipids were not independently related to any of the coronary scores. The LDL triglyceride level, an index of intermediate-density lipoprotein (IDL) accumulation, was significantly correlated to the coronary atheromatosis score in univariate analysis. Nonlipid risk factors were correlated neither to coronary atheromatosis nor to severity of stenoses. Stepwise multiple regression analyses of data adjusted for age, cumulative tobacco consumption, and weight indicated that 18% of the variation in the coronary atheromatosis score could be accounted for by levels of apolipoprotein B. Addition of other lipoprotein variables or the nonlipid variables hypertension and glucose tolerance did not significantly increase the value of R2. When ratios of lipoprotein lipids and apolipoproteins were included in the regression model, the highest multiple correlation coefficient was obtained with the LDL/HDL cholesterol ratio alone (R2 = .22). The present data demonstrate the importance of elevated LDL cholesterol and apolipoprotein B concentrations for the development of coronary atheromatosis in young male survivors of myocardial infarction. The lack of correlations between the levels of lipoprotein lipids and serum apolipoproteins and the severity of coronary stenoses suggests that mechanisms other than disturbances of lipoprotein metabolism may be involved in the progression of more advanced coronary lesions.

Coagulation factor VIII, von Willebrand factor, antithrombin, fibrinogen, plasminogen activator capacity, and inhibitors of fibrinolysis, including a recently discovered fast inhibitor of tissue plasminogen activator, were measured three to six months after myocardial infarction in 116 male and 32 female patients aged less than 45 and in 136 age and sex matched random controls. Plasma concentrations of fibrinogen and the fast inhibitor of tissue plasminogen activator were raised in male patients (with or without correction for orosomucoid levels, blood group distribution, tobacco and alcohol consumption, and weight/height index) and plasminogen activator capacity was reduced. In female patients the concentrations of factor VIII, von Willebrand factor, the fast inhibitor of tissue plasminogen activator, alpha 2-antiplasmin, and C1 inhibitor were significantly increased. The increase in factor VIII concentrations depended strongly on a persisting inflammatory response. Multivariate analysis indicated that a combination of fibrinogen and tissue plasminogen activator inhibitor concentrations gave the best independent discrimination between male patients and controls. For female patients the best combination was von Willebrand factor and tissue plasminogen activator inhibitor. Male patients with multiple vessel atheromatosis at coronary angiography had higher fibrinogen concentrations than those with atheromatosis of a single vessel. Atheromatosis was defined as sharp-edged, plaque-like, or irregular indentations, often multiple, into the vessel lumen without features suggesting fibromuscular hyperplasia.