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Biomedical subjects

A Penttilä

Publications and source records attributed to A Penttilä.

At least 37 records · Page 2Linked to original sources
PubMed2001

Forensic investigations in Kosovo: experiences of the European Union Forensic Expert Team.

The international community has intervened ethnic hostilities in Kosovo, the Federal Republic of Yugoslavia. A team of Finnish forensic experts worked in December 1998 and January 1999 in Kosovo under the mandate of the European Union. The team investigated human remains from three locations of alleged ethnic violence. Concerning the events in Klecka, Volujak and Racak, the International Criminal Tribunal for the former Yugoslavia received documents of great gravity. The standard methods of forensic pathology were complemented with radiological, forensic odontological, physical anthropological and molecular genetic investigations.

Journal Article↗
PubMed2001

Testing genetic susceptibility loci for alcoholic heart muscle disease.

BACKGROUND: Although many heavy alcohol users have subclinical alcoholic heart muscle disease, only a very few develop severe dilated cardiomyopathy. Therefore, and because cardiac abnormalities correlate only weakly with the duration or quantity of drinking, individual susceptibility differences may exist. In this work we examined whether common gene variants previously associated with cardiac hypertrophy or altered alcohol metabolism could modify the effects of alcohol on the heart. METHODS: We studied 700 middle-aged male victims of sudden death who underwent a medicolegal autopsy. In addition to routine postmortem examination, the weights and the cavity and wall dimensions of the left and right ventricle were measured. Coronary artery stenoses were determined from a silicone rubber cast of the arteries. Alcohol consumption and cardiovascular risk factors were assessed by a structured interview of the spouse. The following gene polymorphisms were determined by using polymerase chain reaction restriction fragment length polymorphism and solid-phase minisequencing techniques: angiotensin converting enzyme I/D, angiotensin II type 1 receptor 1166A/C, aldosterone synthase -344C/T, alcohol dehydrogenases 2 and 3, acetaldehyde dehydrogenase 2, and cytochrome P-450 2E1 DraI, PstI, RsaI, and MspI. RESULTS: The most consistent effects of alcohol (p < 0.05) were a higher total heart weight and a larger right ventricle size with increasing daily drinking. However, these and other effects of alcohol were statistically fully independent of the studied genotypes. CONCLUSIONS: The gene polymorphisms selected for and analyzed in our study are unlikely to modify the effects of alcohol on the heart. Other unknown factors determine the individual susceptibility to alcoholic heart muscle disease.

Adult↗
PubMed2001

Dose dependent but non-linear effects of alcohol on the left and right ventricle.

OBJECTIVE: To assess how left (LV) and right ventricular (RV) size, wall thickness, and mass depend on daily alcohol consumption. Among alcoholics, most common findings have been LV hypertrophy and mild systolic or diastolic dysfunction, accompanied occasionally by ventricular dilatation resembling dilated cardiomyopathy. Although it is commonly agreed that chronic heavy alcohol use is injurious to the heart, the dose-injury relation remains a matter of dispute. DESIGN: Prospective series of 700 Finnish men aged 33-70 years who died out of hospital and underwent a medicolegal necropsy. METHODS AND RESULTS: Data on alcohol use and other risk factors were obtained from the spouse. At necropsy, a transversal slice of the heart was traced on a transparent sheet and analysed later for LV and RV cavity areas and wall thicknesses. Coronary artery stenoses were measured from silicone casts of the arteries. In analyses of all men, daily alcohol dose predicted heart weight (beta = 0.17, p < 0.001) and RV cavity area (beta = 0.14, p = 0.007) independent of body size, age, coronary artery disease, hypertension, diabetes, and smoking. In the subgroup of men free of significant coronary artery disease, LV area averaged (SEM) 11.0 (1.0) cm(2) in men drinking < 12 g/day, 7.7 (0.7) cm(2) in those drinking 72-180 g/day, and 10.0 (0.9) cm(2) in those drinking > 180 g/day (p = 0.054). Very heavy drinking (> 180 g/day) was associated with an increase in RV cavity area (p = 0.005). CONCLUSIONS: The effects of alcohol on the heart in middle aged men are dose dependent but partly non-linear. In the absence of coronary artery disease, LV size shows a U shaped reduction with increasing daily alcohol use accompanied by an increase in RV size with very heavy drinking. These findings question the idea of progressive LV dilatation with increasing alcohol consumption among male victims of sudden death.

Adult↗
PubMed2001

Coronary artery complicated lesion area is related to functional polymorphism of matrix metalloproteinase 9 gene: an autopsy study.

Matrix metalloproteinase 9 (MMP9) is expressed in human atherosclerotic plaques, and the protein is localized in human coronary atherosclerotic lesions. The MMP9 gene has a C-to-T promoter polymorphism at position -1562, which affects transcription and leads to promoter low-activity (C/C) and high-activity (C/T, T/T) genotypes. To determine whether these genotypes exert an influence on the atherosclerotic lesion area, we investigated their association with different types of coronary lesions in an autopsy cohort of 276 men aged 33 to 69 years. Areas of the coronary wall covered with fatty streaks and fibrotic, calcified, and complicated lesions were measured, and the percentage of coronary narrowing was determined. MMP9 genotypes were determined by polymerase chain reaction and restriction enzyme digestion. In men aged >/=53 years, the mean area of complicated lesions in 3 coronaries was significantly associated with the MMP9 genotype (P=0.008). Subjects with high promoter activity genotypes had, on average, larger complicated lesion areas than did those with the low-activity genotype. The MMP9 genotype persisted as an independent predictor of complicated lesion area after adjustment for age, body mass index, hypertension, diabetes, and smoking (P=0.012). These data provide evidence that the proposed effect of MMP9 in the process of atherosclerotic lesion development may be modified by the MMP9 genotype.

Adult↗
PubMed2001

Coronary artery disease modifies left ventricular remodelling due to heavy alcohol consumption.

BACKGROUND: Coronary artery disease (CAD) and excessive alcohol use can both damage the myocardium. Their combined effect on the heart muscle has not been characterized. We set out to assess whether the presence of CAD modifies the effects of chronic alcohol consumption on the left ventricular (LV) structure in middle-aged men. METHODS: A postmortem examination was performed on 700 Finnish men (age range, 33-70 years) who experienced a sudden, nonhospital death. A coronary arteriography and measurement of the LV wall thickness, cavity area, and ratio by planimetry of transversal ventricular slices were done at the autopsy. The men were grouped by the most severe coronary artery diameter stenosis (<30%, 30-60%, >60%) and by daily alcohol dose (<12 g, 12-72 g, 72-180 g, >180 g) estimated by a structured interview of their lifetime partner. RESULTS: Analysis by ANCOVA, adjusted for age, body size, smoking, hypertension, and diabetes, showed a statistically significant interaction between the effects of coronary artery stenosis and daily alcohol dose on the LV cavity area (p = 0.037) and on the LV wall thickness/cavity area ratio (p = 0.018). In the group with <30% stenosis, the LV wall thickness/cavity area ratio (mean +/- SEM) increased from 1.6 +/- 0.2 mm/cm2 in men drinking <12 g/day to 6.2 +/- 1.4 mm/cm2 in men drinking 72-180 g/day (p = 0.021). A similar trend was seen in men with 30-60% coronary stenosis (p = 0.32). By contrast, in men with >60% coronary stenosis, the LV wall thickness/cavity area ratio decreased with increasing daily alcohol use from 2.2 +/- 0.3 to 1.4 +/- 0.1 mm/cm2 (p = 0.27). CONCLUSIONS: CAD modulates the effects of alcohol on the heart muscle. Heavy drinking results in concentric LV remodelling in men with no or only mild coronary artery stenoses whereas an opposite trend is seen in men with severe coronary artery obstructions. The mechanism of the interaction remains unknown.

Adult↗
PubMed2001

The role of alcohol in accident and violent deaths in Finland.

BACKGROUND: In Finland, the high rates of forensic autopsy and postmortem toxicology furnish a reliable base for nation-wide studies on alcohol-related violent deaths. MATERIAL AND METHODS: National mortality and population data within Finland, from 1987 to 1996, were used to analyze sex- and age-specific rates, proportions, and trends of violent deaths associated with alcohol. Deaths were defined as alcohol-related when alcohol was certified as a contributing factor to death. RESULTS: During the study period, 10,360 (23.3%) of the 45,544 violent deaths that occurred were alcohol-related. Among 15- to 64-year-olds, 28.6% of accidents, 30.5% of suicides, and 55.3% of homicides were associated with alcohol (alcohol-positive). Differences in epidemiologic patterns and trends for different types of violent death were observed between sexes and age groups. For instance, alcohol-positive accidents significantly decreased in males (-2.3%/year; CL95: -3.3, -1.2; p < 0.001), but not in females (+0.5%/year; CL95: -2.7, +3.7; p = 0.772), and alcohol-positive suicides increased slightly in females (+3.9%/year; CL95: +0.0, +7.9; p = 0.047), but not in males (-0.2%/year, CL95: -1.4, +1.0; p = 0.704). CONCLUSIONS: The victims of violent deaths have often consumed or abused alcohol before the fatal events. Especially in young adults, consumption of alcohol is likely one of the most serious risk factors in accidents and may decrease the threshold for suicide ideation and impulsive behaviors. Studies that explore the effects of sociodemographic and health factors on random populations with relevant control data will increase the understanding of the causal connection between alcohol and violent deaths.

Accidents↗
PubMed2000

Adventitial mast cells connect with sensory nerve fibers in atherosclerotic coronary arteries.

BACKGROUND: The number of activated mast cells is increased in the adventitia of coronary segments with plaque rupture and in spastic atherosclerotic coronary segments. Neurogenic activation of mast cells has been demonstrated previously in other tissues. Here we identified and quantified contacts between mast cells and nerves in the adventitia of normal and atherosclerotic coronary segments. METHODS AND RESULTS: Normal (types 0 or I) and atherosclerotic (lesion types II, III, and IV) coronary segments from 22 unselected autopsy cases were stained for mast cells and sensory nerves by a histochemical double-labeling method. Contacts between mast cells and sensory nerves were quantified morphometrically and also identified by confocal microscopy. Coronary arteries obtained during heart transplantation were stained for the neuropeptides capable of stimulating mast cells, ie, substance P and calcitonin gene-related peptide. In the adventitia of atherosclerotic coronary segments with type IV lesions, the numbers of mast cells and mast cell-nerve contacts (104+/-15 mast cells/mm(2) and 30+/-5 nerve contacts/mm(2); mean+/-SEM) were significantly greater than in segments with type III lesions (79+/-12 [P<0.001] and 24+/-6 [P<0.001]), those with type II lesions (54+/-4 [P<0.001] and 12+/-2 [P<0.001]), or those with normal intima (31+/-3 [P<0.001] and 4+/-1 [P<0.001]). The nerve fibers connected with mast cells contained both substance P and calcitonin gene-related peptide, which identified them as sensory nerves. CONCLUSIONS: Neurogenic stimulation of mast cells in the adventitia of coronary arteries may release vasoactive compounds, such as histamine and leukotrienes, which can contribute to the complex neurohormonal response that leads to abnormal coronary vasoconstriction.

Calcitonin Gene-Related Peptide↗
PubMed2000

Reperfusion injury associated with one-fourth of deaths after coronary artery bypass grafting.

BACKGROUND: This study of reperfusion injury after coronary artery bypass grafting focuses on its contribution to fatal outcome, on its connection with myocardial infarction (MI) and on risk factors. METHODS: A consecutive series of 190 patients (mean age 61.7+/-8.9 years) dying within 30 days following coronary artery bypass grafting was autopsied with concomitant postmortem angiography during 1980 to 1993. RESULTS: Reperfusion injury was revealed in 49 (25.8%) patients, with concomitant MI in almost all (46 of 49) (p < 0.01). Reperfusion injury occurred in association with preoperative New York Heart Association (NYHA) III classification (p < 0.05), coronary endarterectomy (p < 0.01), long aortic clamping time (p < 0.01), and short postoperative survival (p < 0.05). CONCLUSIONS: Reperfusion injury was observed in one fourth of the deaths in association with MI. It occurred more often in patients with preoperative NYHA III symptoms and in those in whom endarterectomy was carried out and the anoxic time of the myocardium was longer. The shorter postoperative survival time indicates the lethal nature of this complication.

Angiography↗
PubMed2000

Glycoprotein IIIa Pl(A1/A2) polymorphism and sudden cardiac death.

OBJECTIVES: We studied the association of the Pl(A1/A2) polymorphism with coronary thrombosis, myocardial infarction (MI) and sudden cardiac death (SCD) in autopsied victims of sudden death. BACKGROUND: Sudden cardiac death is one of the leading symptoms of coronary heart disease in early middle age. Platelet glycoprotein (GP)IIb/IIIa fibrinogen receptors play a key role in coronary thrombosis and MI. Pl(A1/A2) polymorphism of the gene for GPIIIa has been previously studied in hospital MI patients. Significance of the Pl(A1/A2) polymorphism in victims of SCD is not known. METHODS: The Pl(A1/A2) polymorphism was studied in the Helsinki Sudden Death Study comprising 700 autopsied middle-aged white Finnish men (33 to 70 years, mean 53 years) who suffered sudden or violent out-of-hospital death. RESULTS: Prevalence of the A2 allele decreased with age in the series. This decrease was observed among victims of SCD (n = 281) but not in men who died violently (n = 258) or of other diseases (n = 127). Of SCD victims below 50 years, 39.7% were carriers of the A2 allele compared with 28.3% among men under 50 who died of other causes (odds ratio [OR] 2.5, p = 0.01). Men with acute fatal coronary thrombosis (n = 39) were more often (OR 3.4, p < 0.01) carriers of the A2 allele than were men (n = 242) with SCD in the absence of acute coronary thrombosis (48.7% vs. 24.4%, respectively). In addition, men with MI and recent or old thrombosis (n = 67) were more often (OR 3.6, p = 0.005) carriers of the A2 allele than were men (n = 123) with MI in the absence of thrombosis (44.8% vs. 20.3%, respectively). These associations were especially strong in men under 60. CONCLUSIONS: Our results suggest that the A2 allele of the Pl(A1/A2) polymorphism of GPIIIa is a major risk factor of coronary thrombosis and may be one important predictor of SCD in early middle age.

Adult↗
PubMed2000

Plasminogen activator inhibitor-1 (PAI-1) 4G/5G polymorphism, coronary thrombosis, and myocardial infarction in middle-aged Finnish men who died suddenly.

High plasminogen activator inhibitor-1 (PAI-1) plasma levels increase future risk of myocardial infarction (MI). The 4G allele of the 4G/5G polymorphism of the PAI-1 gene has been associated with increased plasma levels of PAI-1. The association of the PAI-1 polymorphism with coronary narrowings, coronary thrombosis and myocardial infarction (MI) was studied in a prospective autopsy series of 300 middle-aged Caucasian Finnish men (33 to 69 yrs) suffering sudden out-of-hospital death (Helsinki Sudden Death Study). The 4G allele was found in 76.8% of men with sudden cardiac death (SCD) compared to 67.5% in men who died accidentally and 63.2% in men who died of other diseases (p = 0.08 and p = 0.055, respectively). Men possessing the 4G allele had more often acute MI (OR 3.5; p <0.05) and coronary thrombosis (OR 5.5. p = 0.01) compared to 5G homozygotes. 5G homozygotes, comprising one third of the men in our study, seem to be at a decreased risk of thrombosis, whereas carriers of the common 4G allele have an increased risk of thrombosis, AMI and possibly SCD compared to 5G homozygotes.

Accidents↗
PubMed1999

The GPIIIa Pl(A) polymorphism in the progression of abdominal aortic atherosclerosis.

Glycoprotein IIIa is expressed in platelets as part of the fibrinogen receptor and also in vascular endothelium where it mediates smooth muscle cell proliferation. The association between the glycoprotein GPIIIa Pl(A) polymorphism and the stage of atherosclerosis in the abdominal aorta was studied in a prospective autopsy study series of 300 middle-aged men (33-69 years). The Pl(A) genotype was determined by RFLP-PCR. The stage of atherosclerosis in the abdominal aorta was determined by computer-assisted morphometry. Elevated, fibrous lesions were more frequently (P=0.05) found in the abdominal aortas of men with the Pl(A1) homozygous genotype compared to men with the A2 allele (OR 2.3; 95% CI 0.99-5.2). The area of complicated lesions was significantly greater in men with Pl(A2)-positive genotypes compared to A1 homozygotes. The association with complicated lesions was especially strong in men over 60 (P=0.002). These results suggest that Pl(A) polymorphism is involved in the progression of atherosclerosis in the abdominal aorta. The association of men possessing the Pl(A2) allele with slower development of fibrous lesions and with greater area of complicated lesions in the abdominal aorta may result from genotypic differences in the smooth muscle cell proliferation after slight injuries to the endothelium mediated by glycoprotein IIIa or from genotypic differences in platelet fibrinogen binding or both.

Adult↗
PubMed1999

Age-dependent association of apolipoprotein E genotype with coronary and aortic atherosclerosis in middle-aged men: an autopsy study.

BACKGROUND: Apolipoprotein E (apoE) polymorphism is one of the genetic determinants of serum cholesterol values. The apoE epsilon4 allele has been associated with advanced coronary heart disease (CHD) diagnosed by angiography, but the role of the apoE genotype in atherosclerosis has not been confirmed at vessel-wall level, nor is any age-dependent effect of the apoE genotype on the development of CHD known. METHODS AND RESULTS: The right and left anterior descending coronary arteries (RCA and LAD) and the aorta from 700 male autopsy cases (Helsinki Sudden Death Study) in 1981-1982 and 1991-1992 (average age 53 years, range 33 to 70 years) were stained for fat, and all areas covered with fatty streaks, fibrotic plaques, and complicated lesions were measured. In the RCA and LAD, the apoE genotype was significantly associated with the area of total atherosclerotic lesions in men <53 years old but not with that in older men (P=0.0085 and P=0.041, respectively, for age-by-genotype interaction). Men <53 years old with the epsilon4/3 genotype showed 61% larger total atherosclerotic lesion area in the RCA (P=0.0027) and 26% larger area in the LAD (P=0.12) than did men with the epsilon3/3. The apoE epsilon4/3 was also associated with atherosclerotic lesions in the abdominal (P=0.014) and thoracic (P=0.12) aorta, but this effect, unlike that of the coronary arteries, was not age-related. CONCLUSIONS: In men, the apoE epsilon4 allele is a significant genetic risk factor for coronary atherosclerosis in early middle age. This suggests that at older age, other known risk factors of CHD play a more important role in the atherosclerotic process than apoE polymorphisms.

Age Factors↗
PubMed1999

Association between myocardial infarction and the mast cells in the adventitia of the infarct-related coronary artery.

BACKGROUND: Histamine, a product of mast cells, is an effective vasoconstrictor of atherosclerotic coronary arteries. Because it has been suggested that coronary spasm plays a role in acute coronary syndromes such as myocardial infarction (MI), we quantified and characterized the mast cells in the adventitia of infarct-related coronary arteries. METHODS AND RESULTS: In a series of 17 autopsied MI patients, we identified the segment of the left coronary artery with ruptured plaque responsible for the infarction. More distal segments from the infarct-related coronary artery, either with nonruptured plaques or with normal intima, were also studied. Corresponding segments taken from left coronary arteries obtained from 17 patients who had died of noncardiac causes served as controls. Adventitial mast cells in the infarct-related and the control coronary arteries were identified immunohistochemically by staining for tryptase. In the infarct-related coronary arteries, we also stained for chymase and histamine. Moreover, T lymphocytes and macrophages were identified immunohistochemically and counted. In the infarct-related coronary arteries, significantly larger numbers of mast cells were present in the adventitia backing ruptured plaques (98+/-40 mast cells/mm2, mean+/-SD) than in the adventitia backing nonruptured plaques (41+/-12 mast cells/mm2; P<0.001) or backing normal intima (19+/-8 mast cells/mm2; P<0.001). No such difference was found among the 3 different segments in the control coronary arteries. The majority of mast cells contained not only tryptase but also chymase. Mast cells were the only cells in the coronary adventitia that contained histamine. The proportion of adventitial mast cells that were degranulated was highest in the segments with ruptured plaques. The numbers of adventitial macrophages and T lymphocytes were also increased in the segments with plaque rupture. CONCLUSIONS: In infarct-related coronary arteries, the number of degranulated mast cells in the adventitia backing ruptured plaques is increased. Histamine released from the degranulated mast cells may reach the media, where it may locally provoke coronary spasm and thus contribute to the onset of MI.

Aged↗
PubMed1999

Post-mortem cast angiography in the diagnostics of graft complications in patients with fatal outcome following coronary artery bypass grafting (CABG).

The advantages and limitations of a novel post-mortem angiographic method using solidifying silicone rubber and lead oxide as a contrast medium in detecting coronary artery graft complications on a routine basis were evaluated in a series of 223 consecutive patients with fatal outcome within 30 days following coronary artery bypass grafting (CABG). Of these patients, 166 (74.4%) were male and 57 (25.6%) female (mean age 61.9 +/- 9). Coronary grafts totalled 660 (3.0 per patient) with 517 aortic and 838 coronary anastomoses. At autopsy, the rubber cast model of the grafts and coronary arterial tree was exposed by a bend scalpel and sites of possible complications were examined. Post-mortem angiographs were re-evaluated and compared with preoperative angiographs and dissection findings. By combining the findings of angiography and heart dissection, 122 (54.7%) of the 223 patients were found to have some type of complication of the graft or the anastomosis. The diagnostic sensitivity and specificity of post-mortem angiography was 100% in assessing narrowing or twisting of the graft as well as narrowing of the aortal anastomosis, whereas these findings were revealed with difficulty by autopsy dissection only. In cases with correct x-ray projection, narrowing and occlusion of the proximal aortal and distal coronary anastomosis were also reliably revealed by angiography. In contrast, graft thrombosis was clearly overdiagnosed by angiography, leading to a lower specificity (84%) but high sensitivity (100%) in detecting this complication. Post-mortem angiography also failed to detect dissection of the wall of the graft or anastomosis. Technical problems with this angiographic method were due to too low perfusion pressure, too rapid polymerizing of the silicone rubber, leakage of contrast medium into the ventricles, or faulty x-ray projections. These results suggest that our post-mortem angiographic technique, yielding a permanent rubber-cast model of the graft and anastomosis site, improves the accuracy of diagnostics of postoperative CABG complications and eases postoperative autopsy dissection, which can now be directed to confirm suspected complications.

Aged↗
PubMed1999

Association of FXIII Val34Leu with decreased risk of myocardial infarction in Finnish males.

Factor XIII is a transglutaminase that crosslinks fibrin in the last steps of the coagulation process. A few polymorphic sites have been identified in this gene, one of them being a point mutation (FXIII Val34Leu), leading to an amino acid change of valine to leucine. Recently, in British patients, FXIII 34Leu allele was suggested to be associated with a decreased incidence of myocardial infarction (MI). PAI-1 4G/4G genotype seemed to lessen the beneficial effect of FXIII 34Leu allele. The aim of our study was to further investigate the possible protective role of the FXIII 34Leu allele against MI and its suggested interaction with the PAI-1 4G/5G polymorphism. We carried out genotype analyses for FXIII Val34Leu using solid-phase minisequencing in two independent Finnish study groups. In our study, the FXIII 34Leu allele was associated with a lower risk of MI (P = 0.009), however, the PAI-1 4G allele showed no interaction with this polymorphism. To establish the population frequency of the FXIII 34Leu allele and to study the possible variations in Finland four DNA pools from different geographical areas of Finland were genotyped. No significant differences in the allele frequencies were observed (21-28%) except in the Eastern Kainuu area (13%), an area with an increased risk of mortality from coronary artery disease (CAD), supporting the results presented above. The association of FXIII 34Leu variant with a lower incidence of myocardial infarction suggests a new role for FXIII in a polygenic thrombotic disease.

Alleles↗
PubMed1999

Glycoprotein IIIa Pl(A) polymorphism associates with progression of coronary artery disease and with myocardial infarction in an autopsy series of middle-aged men who died suddenly.

Glycoprotein IIIa (GPIIIa) has a key role in the aggregation of thrombocytes, and it also mediates intimal hyperplasia after endothelial injuries; the possible association of the Pl(A1/A2) polymorphism of the gene for GPIIIa with coronary thrombosis and with the progression of coronary artery disease (CAD) is still to be confirmed. Therefore, the association of the Pl(A) polymorphism with the development of coronary atherosclerosis, coronary narrowing, and myocardial infarction (MI) was studied in a prospective, consecutive autopsy series of 300 middle-aged, white Finnish men (33 to 69 years) suffering sudden out-of-hospital or violent death. Coronary atherosclerosis was measured morphometrically and the coronary stenosis percentage determined from a cast rubber model of the coronary tree. We found a significant inverse relation (P=0.01) between the Pl(A2)-positive genotype and coronary artery stenosis. The frequency of possessing the Pl(A2) allele was significantly (odds ratio [OR] 0.45, 95% confidence interval [CI] 0.22 to 0.98) lower among men with >50% coronary stenosis (18.3%) than among those with <25% stenosis (32.9%). Although the Pl(A) polymorphism was not directly associated with MI, the Pl(A2) allele was present in 11 of the 22 men (50%) with MI and coronary thrombosis (OR 6.6, 95% CI 2.1 to 22.8) but in only 6 of the 47 (12.8%) with MI associated with severe stenosis in the absence of thrombosis. In line with this result, men possessing the Pl(A2) allele also had a larger area of fissured and ulcerated complicated lesions in their coronary arteries (P<0.05). The present results suggest that the Pl(A) polymorphism is involved in the development of CAD and MI. Men with the Pl(A2) allele may harbor more thin-walled, vulnerable coronary plaques, plaques prone to rupture, leading to massive, fatal thrombosis. In contrast, men homozygous for the Pl(A1) allele may more often show stable plaques and present with infarction caused by progressive coronary stenosis.

Adult↗