Sex-based differences in outcomes with bivalirudin or unfractionated heparin for transcatheter aortic valve replacement: Results from the BRAVO-3 randomized trial.

BACKGROUND: Women comprise almost 50% of patients undergoing transcatheter aortic valve replacement (TAVR) and previous studies have indicated higher rates of procedural complications and bleeding in women compared to men. It is unknown whether men and women demonstrate a differential response to bivalirudin versus unfractionated heparin (UFH) in TAVR. We sought to evaluate outcomes by sex and type of anticoagulant from the Bivalirudin Versus Heparin Anticoagulation in Transcatheter Aortic Valve Replacement (BRAVO-3) trial of transfemoral TAVR. METHODS: BRAVO-3 was a randomized multicenter trial comparing transfemoral TAVR with bivalirudin versus UFH (31 centers, n = 802). The primary endpoint was 48 h major bleeding defined as Bleeding Academic Research Consortium (BARC) type ≥3b. Major adverse cardiovascular events (MACE) were a composite of 30-day death, myocardial infarction, or stroke. Net adverse cardiovascular events (NACE) were a composite of BARC ≥3b bleeding or 30-day MACE. We examined the outcomes in men and women. RESULTS: The total cohort included 49% women (n = 391, 195 received bivalirudin and 196 UFH) and 51% men (n = 411, 209 received bivalirudin and 202 UFH). Women were older than men with fewer comorbidities including coronary artery disease, atrial fibrillation, diabetes but similar EuroSCORE I. Women received smaller sheath and device sizes compared with men without differences in the use of vascular closure devices. At 48-hr post-TAVR there was no difference in bleeding or vascular complications in women compared to men. The use of bivalirudin did not result in significantly lower bleeding at 48 hr or 30-days compared to UFH. CONCLUSIONS: There was no difference in early outcomes with bivalirudin versus UFH in men or women undergoing contemporary TAVR. © 2016 Wiley Periodicals, Inc.

Large scale association analysis of novel genetic loci for coronary artery disease.

BACKGROUND: Combined analysis of 2 genome-wide association studies in cases enriched for family history recently identified 7 loci (on 1p13.3, 1q41, 2q36.3, 6q25.1, 9p21, 10q11.21, and 15q22.33) that may affect risk of coronary artery disease (CAD). Apart from the 9p21 locus, the other loci await substantive replication. Furthermore, the effect of these loci on CAD risk in a broader range of individuals remains to be determined. METHODS AND RESULTS: We undertook association analysis of single nucleotide polymorphisms at each locus with CAD risk in 11,550 cases and 11,205 controls from 9 European studies. The 9p21.3 locus showed unequivocal association (rs1333049, combined odds ratio [OR]=1.20, 95% CI [1.16 to 1.25], probability value=2.81 x 10(-21)). We also confirmed association signals at 1p13.3 (rs599839, OR=1.13 [1.08 to 1.19], P=1.44 x 10(-7)), 1q41 (rs3008621, OR=1.10 [1.04 to 1.17], P=1.02 x 10(-3)), and 10q11.21 (rs501120, OR=1.11 [1.05 to 1.18], P=4.34 x 10(-4)). The associations with 6q25.1 (rs6922269, P=0.020) and 2q36.3 (rs2943634, P=0.032) were borderline and not statistically significant after correction for multiple testing. The 15q22.33 locus did not replicate. The 10q11.21 locus showed a possible sex interaction (P=0.015), with a significant effect in women (OR=1.29 [1.15 to 1.45], P=1.86 x 10(-5)) but not men (OR=1.03 [0.96 to 1.11], P=0.387). There were no other strong interactions of any of the loci with other traditional risk factors. The loci at 9p21, 1p13.3, 2q36.3, and 10q11.21 acted independently and cumulatively increased CAD risk by 15% (12% to 18%), per additional risk allele. CONCLUSIONS: The findings provide strong evidence for association between at least 4 genetic loci and CAD risk. Cumulatively, these novel loci have a significant impact on risk of CAD at least in European populations.

Cardiovascular phenotypes and functional parameters in the general population--results of the MONICA/KORA studies.

The MONICA/KORA surveys are characterized by a careful and broad investigation of multiple cardiovascular phenotypes. Particularly, repeated blinded measurements of blood pressure, comprehensive echocardiographic and electrocardiographic evaluations as well as differentiation between fat and fat-free body mass have led to manifold innovative observations. Specifically, genetic and serological markers of the renin angiotensin system could be associated with high blood pressure and left ventricular hypertrophy. The same applies to the importance of parameters of body composition as obesity and muscular mass. Moreover, the prevalence of heart failure in the general population could be determined for the first time in Germany. Additionally, the prevalence of left ventricular systolic and diastolic dysfunction could be obtained in the region of the survey, exemplarily for the Federal Republic of Germany. Finally, the surveys of the population random sample were used to define normal serum levels of natriuretic peptides. In summary, the evaluation of cardiovascular phenotypes in the MONICA/KORA surveys resulted in a -- in the European region unique -- documentation of cardiovascular functional parameters in the general population. Moreover, multiple epidemiological observations as to pathophysiologically relevant topics of heart and vascular diseases could be studied in extraordinary details.

Failure to achieve recommended LDL cholesterol levels by suboptimal statin therapy relates to elevated cardiac event rates.

OBJECTIVES: The majority of patients with myocardial infarction (MI) and hypercholesterolaemia does not achieve guideline recommended low-density lipoprotein cholesterol (LDL) levels. Suboptimal dosages of statins explain this dilemma in most patients. DESIGN AND SETTING: We evaluated the relationship between statin treatment quality (optimal: LDL<115 mg/dl, suboptimal: LDL>/=115 mg/dl, no statin therapy despite hypercholesterolaemia) and the subsequent incidence of coronary events (coronary death, nonfatal MI, bypass surgery) over a 30 months follow-up in a large cohort of post MI patients with hypercholesterolaemia (n=2045). Analysis was performed in a nested case-control manner comparing 173 cases with a coronary event and 346 matched controls. RESULTS: Patients who developed a coronary event were treated optimally in 11.0%, suboptimally in 43.4% (p<0.05 vs. optimal treatment) and were untreated in 45.7% (p<0.001 vs. optimal treatment). Respective numbers in event-free patients were 21.4%, 47.7%, and 30.9%. After adjustment for most potential confounders, including all cardiovascular risk factors and medication, the relative risk of future non-fatal MI and coronary death associated with a suboptimal statin treatment was 2.02 (95% CI 1.04 to 4.18) compared to optimal statin treatment. Moreover, the statin equivalent dose in optimally treated individuals was significantly higher than in suboptimally treated individuals (0.85+/-0.03 vs. 0.78+/-0.02, p<0.05). CONCLUSION: In this community-based study, a lipid lowering therapy with statins into the recommended target range of LDL levels may be associated with decreased cardiovascular risk compared to a statin therapy without titrating the LDL level below 115 mg/dl. Thus, the quality of statin treatment was identified as an independent predictor of coronary events in post MI patients.

Sudden cardiac death in myotonic dystrophy type 2.

Medical records and follow-up data were reviewed in 297 genetically proven myotonic dystrophy type 2 (DM2) patients. Patients were selected by the criteria of cardiac sudden death before age 45. Sudden death occurred in four patients, three of whom were cardiological asymptomatic, and one with a history of heart failure. Cardiac histopathology showed dilated cardiomyopathy in all, and conduction system fibrosis in two patients. Pathogenetic CCUG ribonuclear inclusions were demonstrable in cardiomyocytes.

KCNJ11 polymorphisms and sudden cardiac death in patients with acute myocardial infarction.

PURPOSE: Patients with an acute myocardial infarction (AMI) are of high risk to develop ischemia-induced ventricular arrhythmias, leading to sudden cardiac death (SCD) in about one third of all AMI patients. The individual susceptibility to ischemia-induced arrhythmias may be modified by polymorphisms in genes encoding ion channels. The cardiac ATP-dependent potassium channel (K(ATP)) current is generated by ion channels encoded by the KCNJ11 gene and the SUR2a gene. Opening of the K(ATP) channel during ischemia results in action potential shortening in various studies and may therefore influence the outcome of AMI patients. METHODS: Using a three-primer strategy, we sequenced the complete coding and adjacent 5' and 3' sequences of the intronless KCNJ11 gene (1.3 kb) prospectively in two groups. Patients of group 1 (n = 84) survived three or more transmyocardial infarctions without developing any ventricular arrhythmias. Patients of group 2 died suddenly from their first myocardial infarction (n = 86), most of them witnessed SCDs. RESULTS: We identified a total of six known polymorphisms (K23E, A190A, L267V, L270V, I337V, and K281K) and two new polymorphisms (L267L, 3'UTR +62 G/A). The allele, genotype, and haplotype frequencies did not differ between the two groups. All polymorphisms were found to be in Hardy-Weinberg equilibrium. In addition, we identified two novel missense mutations in a highly conserved region of the gene in two patients of group 2 (P266T and R371H) with yet unknown functional consequences. CONCLUSION: In this study of AMI patients, SCD was not related to polymorphisms in the KCNJ11 gene.

Prevalence of left ventricular diastolic dysfunction in the community. Results from a Doppler echocardiographic-based survey of a population sample.

AIMS: The prevalence of left ventricular diastolic abnormalities in the general population is largely unclear. Thus, the aim of this study was, firstly, to identify abnormal diastolic function by echocardiography in an age-stratified population-based European sample (MONICA Augsburg, n=1274, 25 to 75 years, mean 51+/-14) and, secondly, to analyse clinical and anthropometric parameters associated with diastolic abnormalities. METHODS AND RESULTS: The overall prevalence of diastolic abnormalities, as defined by the European Study Group on Diastolic Heart Failure (i.e. age dependent isovolumic relaxation time (92-105 ms) and early (E-wave) and late (A-wave) left ventricular filling (E/A-ratio, 1-0.5)) was 11.1%. When only subjects treated with diuretics or with left atrial enlargement were considered (suggesting diastolic dysfunction) the prevalence was 3.1%. The prevalence of diastolic abnormalities varied according to age: from 2.8% in individuals aged 25-35 years to 15.8% among those older than 65 years (P<0.01). Significantly higher rates of diastolic abnormalities were observed in men as compared to women (13.8% vs 8.6%, P<0.01). Independent predictors of diastolic abnormalities were arterial hypertension, evidence of left ventricular (LV) hypertrophy, and coronary artery disease. Interestingly, in the absence of these predisposing conditions, diastolic abnormalities (4.3%) or diastolic dysfunction (1.1%) were rare, even in subjects older than 50 years of age (4.6%) and (1.2%), respectively. In addition to these factors, diastolic dysfunction was related to high body mass index, high body fat mass, and diabetes mellitus. CONCLUSION: The prevalences of diastolic abnormalities and diastolic dysfunction are higher than that of systolic dysfunction and are increased (despite age-dependent diagnostic criteria) in the elderly. However, in the absence of risk factors for diastolic abnormalities or diastolic dysfunction, namely LV hypertrophy, arterial hypertension, coronary artery disease, obesity and diabetes the condition is rare even in elderly subjects. These data allow speculation on whether diastolic heart failure may be prevented by improved implementation of measures directed against predisposing conditions.

Do siblings of myocardial infarction patients have a specific management of hypertension?

The aim of this study was to determine whether the management of hypertension differs between siblings of myocardial infarction patients and the general population. Siblings aged 35 to 74 years, unaffected by myocardial infarction, were drawn from the Augsburg Family Heart Study, conducted in 1996-1997 in southern Germany (n = 524). The reference group consisted of participants of the third MONICA population-based survey conducted in 1994-1995 in the same area, who were aged 35 to 74 years and also unaffected by myocardial infarction (n = 3802). Prevalence, awareness, treatment and control of hypertension (defined by blood pressure > or = 140/90 mm Hg or use of antihypertensive medication) were compared between the two groups. The result was that the prevalence of hypertension was higher in the siblings (men: age-adjusted OR = 1.31, 95% CI: 0.99-1.75; women: age-adjusted OR = 1.83, 95% CI: 1.39-2.41). Male hypertensive siblings were more often aware and treated for hypertension than male hypertensives of the reference group whereas the level of awareness and treatment was comparable between female hypertensives of the two groups. In both genders, no difference in the degree of control was shown between hypertensives of the two groups. In conclusion the siblings and their physicians should pay more attention to the family history of myocardial infarction in order to improve the management of hypertension in this high risk group.

[Inpatient rehabilitation improves implementation of therapeutic guidelines for secondary prevention in patients with coronary heart disease]. / Die stationäre Rehabilitation verbessert die Umsetzung der Therapierichtlinien zur Sekundärprävention bei Patienten mit koronarer Herzerkrankung.

In Germany, measures for secondary prevention in patients with coronary artery disease are poorly utilized. We therefore investigated whether a cardiac in-hospital rehabilitation and education program may enhance the implementation of respective guidelines in patients with severe coronary artery disease (CAD). Specifically, we developed a case-control design in siblings with severe CAD in order to achieve optimal matching for patients with or without participation in the rehabilitation program. By the screening of more than 200,000 patient charts in 15 cardiac rehabilitation clinics, we identified 1500 families in which at least two siblings suffered from severe coronary artery disease. In 268 such sibling pairs, siblings were discordant with respect to participation in a 3-4 week cardiac in-hospital rehabilitation program. The coronary risk profile was studied, first, retrospectively at the time of hospitalization for acute MI or revascularization procedures and, secondly, prospectively at the time of follow-up (on average 5.2 years later). At the time of the acute cardiac event, both groups showed an equal risk factor distribution suggesting appropriate matching. However, at follow-up the number of individuals taking antihypertensive medication and displaying effective antihypertensive treatment (< or = 140/90 mmHg) was significantly higher in the rehabilitation group (92.2 vs. 82.1%, p < 0.01; 59.7 vs. 37.2%). Accordingly, rehabilitation siblings presented with significantly lower systolic (137 +/- 1 vs. 145 +/- 1 mmHg; p < 0.01) and diastolic blood pressure (82 +/- 1 vs. 85 +/- 1 mmHg; p < 0.01). The utilization of CSE inhibitors was also significantly higher in siblings participating in the rehabilitation program (57.5 vs. 43.1%; p < 0.01), leading to significantly lower blood lipid levels in these siblings (total cholesterol 225 +/- 3 vs. 236 +/- 3 mg/dL, p < 0.01; LDL cholesterol 148 +/- 3 vs. 158 +/- 3 mg/dL, p < 0.01). Moreover, participation in the cardiac rehabilitation stimulated markedly more smokers to quit (80.8 vs. 57.6%, p < 0.01). Additionally, there was a strong temporal trend from 1997 until 2000 towards improved control of arterial hypertension in rehabilitation siblings. In parallel, the utilization of CSE inhibitors increased over time and LDL cholesterol decreased. These favorable temporal trends were also observed in siblings not participating in the rehabilitation program, however, to a lesser extent. Taken together, in the last four years, the implementation of secondary preventive strategies in patients with cardiac disease improved. Siblings who participated in a rehabilitation program displayed a better control of cardiovascular risk factors as compared to those not participating in such a program. Thus, an in-hospital cardiac rehabilitation program may successfully encourage the implementation of measures for secondary prevention and enhance the treatment of coronary risk factors.

Siblings of myocardial infarction patients are overlooked in primary prevention of cardiovascular disease.

AIMS: Patients with arterial hypertension or hypercholesterolaemia may benefit from medical therapy for primary prevention of myocardial infarction. Preventive therapy may be particularly effective in individuals with a positive family history for myocardial infarction since such subjects are at high risk for coronary events. The objective of this population-based study was to analyse the risk profile as well as the current utilization of preventive strategies in asymptomatic siblings of patients with myocardial infarction. METHODS AND RESULTS: We studied siblings of 325 patients with premature myocardial infarction from the Augsburg MONICA myocardial infarction registry by standardized questionnaire, blood pressure recordings, and biochemical measurements. Out of 580 siblings, 510 were free of coronary heart disease symptoms. With multiple risk factors being present in most asymptomatic siblings, 29.4% of asymptomatic individuals had an estimated individual 10-year risk for a major cardiovascular event of > or = 20%, or when projected to the age of 60. According to the guidelines of the European Societies of Cardiology, Atherosclerosis, and Hypertension (ESC/EAS/ESH) from 1994 (1998 guidelines in parenthesis) dietary and lifestyle interventions were indicated for arterial hypertension in 48.1% (43.0%) and/or for hypercholesterolaemia in 17.3% (78.8%). Drug treatment was indicated for arterial hypertension in 27.9% (30.6%) and for hypercholesterolaemia in 13.6% (19.1%) of asymptomatic siblings. Of those individuals with the respective indication, actual drug treatment was given for arterial hypertension in 91.5% (83.3%) and for hypercholesterolaemia in 46.4% (33.0%). However, treatment targets were reached in only 31.0% (28.2%) with arterial hypertension and in 7.2% (5.2%) with hypercholesterolaemia, respectively. CONCLUSIONS: Most asymptomatic individuals with positive fraternal family history have more than one modifiable risk factor. Interestingly, a large number of these individuals appears to be under medical surveillance as many receive some sort of drug treatment. However, this therapy did not meet the treatment goals in the majority of those with arterial hypertension and/or hypercholesterolaemia. Thus, although individuals with a positive fraternal history for myocardial infarction can be easily identified, implementation of sufficient preventive strategies continues to be poor in a Western European country.

Long-term effects of in-hospital cardiac rehabilitation on the cardiac risk profile. A case-control study in pairs of siblings with myocardial infarction.

AIMS: In the general population, measures for secondary prevention of myocardial infarction are poorly utilized. Our aim was therefore to analyse whether post-myocardial infarction in-hospital rehabilitation and education programmes improve the subsequent utilization of preventive strategies. METHODS AND RESULTS: We screened 93 500 patient charts in cardiac rehabilitation clinics to identify a myocardial infarction patient with a sibling, who likewise had a myocardial infarction prior to the age of 60 years but was discordant with respect to the participation in cardiac in-hospital rehabilitation. In 92 such sibling pairs the coronary risk profile was studied by standardized questionnaire, biochemical measurements and physical examination. At the time of the acute myocardial infarction, both groups showed an equal risk factor distribution. However, at follow-up (on average 5.5 years after myocardial infarction), rehabilitation-siblings presented with significantly lower systolic (137+/-2 vs 150+/-3 mmHg, P<0.01) and diastolic blood pressure (82+/-1 vs 89+/-1 mmHg, P<0.01). Antihypertensive drug therapy resulted more often in effective (

The D-allele of the ACE polymorphism is related to increased QT dispersion in 609 patients after myocardial infarction.

AIMS: Prolongation of QT dispersion can be observed in some patients with myocardial infarction and serves as a possible independent risk factor for sudden cardiac death. Angiotensin-converting enzyme (ACE) inhibition has been shown to reduce QT dispersion in myocardial infarction patients. We hypothesized that ACE gene I/D polymorphism, which is known to modulate ACE activity, may also affect QT dispersion after myocardial infarction. METHODS AND RESULTS: We studied 609 myocardial infarction patients (532 men, aged 56.1+/-0.3; mean 5.5 years after myocardial infarction) from a population-based myocardial infarction register by standardized questionnaire, anthropometry, ECG, echocardiography, and genotyping of ACE I/D polymorphism. In addition, 540 unaffected siblings (251 men, age 54.6+/-0.4 years) of these patients were studied by the same protocol. As compared with their healthy siblings, mean QT dispersion was prolonged in myocardial infarction patients (65.9+/-1.4 ms vs 91.2+/-2.3 ms, respectively, P<0.001). QT dispersion was negatively correlated to left ventricular ejection fraction (P<0.005). The ACE DD-genotype was associated with longer QT dispersion in myocardial infarction patients (103.0+/-4.6 ms vs 81.9+/-4.5 ms in the II group, P<0.001). This association was noted to be strong in multivariate analyses that included age, gender, ejection fraction, left ventricular end-diastolic diameter, medication, and heart rate. In contrast, no association between the ACE DD-genotype and QT dispersion was detected in healthy siblings of myocardial infarction patients. CONCLUSION: Thus, the ACE D-allele may be associated with increased QT dispersion in patients after myocardial infarction but not in healthy subjects. An interaction of myocardial damage and genetic predisposition that both enhance the activity of the renin angiotensin system may decrease the repolarization homogeneity of the heart.

[ACE inhibition in patients with myocardial infarct and ventricular dysfunction: inappropriate application of therapy standards in patient samples]. / ACE-Inhibition bei Myokardinfarktpatienten mit eingeschränkter Ventrikelfunktion: Umsetzung von Therapiestandards in Bevölkerungsstichproben.

Several reports indicate the benefit of ACE inhibitors for patients with left ventricular systolic dysfunction after acute myocardial infarction (MI). We sought to determine the implementation of the treatment guidelines in patient samples from the general population. Furthermore we aimed to identify patient characteristics associated with the use of ACE inhibitors. Screening of two MI-registries allowed the identification of 226 MI patients with left ventricular dysfunction. Patients were considered to be eligible for ACE inhibitor therapy when a EF < or = 40% was documented in the patient records of cardiac rehabilitation clinics (REG-MI, n = 147) or detected by standardised echocardiography (KORA, n = 78). On average 5.5 years following MI, a standardised questionnaire and a detailed medical history was obtained. Specifically, information was collected regarding current medication and potential contraindications for ACE inhibitors. MI patients with LV dysfunction received ACE inhibitors in 62% (REG-MI) and 45% (KORA). The doses prescribed were substantially smaller than target doses used in the large-scale studies (REG-MI: 40 +/- 4%, KORA: 23 +/- 3%, % of target doses). Only 13% (REG-MI) and 3% (KORA) received more than 50% of the target dosage. Additionally, actual doses of the most frequently used ACE inhibitors were significantly different (captopril: 23 +/- 2%, enalapril: 42 +/- 5% of target doses). The likelihood of receiving ACE inhibitors was significantly higher in patients with written recommendation for such medication (odds ratio 6.02, confidence interval 1.93-20.16) and in patients visiting cardiologists (odds ratio 3.69, confidence interval 1.26-11.07) as revealed by multivariate analysis of the REG-MI database. Despite national and international guidance, a large proportion of MI patients with left ventricular dysfunction is not receiving ACE inhibitors, and when used, the doses prescribed are markedly smaller than target doses used in clinical trials that established the utility of these drugs. Medical care by cardiologists and written recommendation of ACE inhibition in patient records were independent predictors of a more appropriate prescription of ACE inhibitors.

Marked suppression of renin levels by beta-receptor blocker in patients treated with standard heart failure therapy: a potential mechanism of benefit from beta-blockade.

OBJECTIVES: Recent trials demonstrated beneficial effects of beta-blockers in combination with standard heart failure medication. The mechanisms underlying this benefit are incompletely understood. We hypothesized that beta-blockers may augment the inhibition of the renin-angiotensin system in patients with left ventricular (LV) dysfunction treated with angiotensin-converting enzyme (ACE) inhibitors and/or diuretics by prevention of renin upregulation that occurs in such patients. DESIGN: We examined plasma renin levels (direct radioimmunometric assay) in 312 men with previous myocardial infarction (MI) and echocardiographic LV dysfunction. Patients took medication according to their physicians' prescriptions: antiplatelet agents alone (n=62) or in combination with ACE inhibitors, diuretics or beta-blockers (n=250). RESULTS: Plasma renin levels were elevated in patients taking ACE inhibitors or diuretics and ACE inhibitors plus diuretics (adjusted means from multiple regression analysis were 28.5 mU L-1 [95% CI=20.6-39.5] and 73.7 mU L-1 [95% CI = 49.9- 109.9], respectively) compared with patients on antiplatelets alone (16.1 mU L-1, 95% CI = 13.5-19.3, P < 0.05 each). The combinations of beta-blockers with ACE inhibitors or diuretics and beta-blockers with ACE inhibitors plus diuretics were related to markedly suppressed plasma renin levels (adjusted means 16.4 [13.1-20.6] and 32.1 [23.3-44.3]) as compared with respective patient groups without beta-blockers (P < 0.01 each). CONCLUSIONS: Concomitant beta-blocker treatment can prevent the reactive renin stimulation and potentially the escape from effective inhibition of the renin-angiotensin system in patients with LV dysfunction after MI treated with ACE-inhibitors and/or diuretics.

Association between a polymorphism in the G protein beta3 subunit gene (GNB3) with arterial hypertension but not with myocardial infarction.

OBJECTIVE: A polymorphism at position 825(C-->T) of the G protein beta3 (GNB3) gene was found to be associated with enhanced transmembrane signalling as well as with an increased prevalence of arterial hypertension. The aim of the present study was to further investigate the association of the GNB3 C825T allele status with arterial hypertension in a large population-based sample and its association with specific end organ damage, i.e. myocardial infarction (MI). METHODS: Individuals from a population-based sample (n=2052) and patients suffering from premature MI (age at first MI < or = 60 years, n = 606) were studied by questionnaire as well as by physical examination and biochemical analyses. RESULTS: In the population-based sample, the prevalence of arterial hypertension (blood pressure > or = 160/95 mmHg and/or antihypertensive medication) was higher in individuals with the TT genotype (41.8%) as compared to heterozygote individuals (36.6%) or those with the CC genotype (32.75%) (P = 0.02). This association was predominantly found in men. Moreover, men without antihypertensive medication carrying the TT genotype showed higher diastolic blood pressure than those carrying the CC genotype (86.5 vs. 83.7 mmHg, P = 0.04). However, the genotype distribution and the allele frequencies were similar in both, the population-based and the MI patient sample. Furthermore, neither the age at the time of MI nor the location of the MI were related to the genotype distribution. Similarly, gender and age stratified analyses did not show any association of the GNB3 genotype and MI. CONCLUSIONS: In male individuals from a large population-based sample, the T allele of the GNB3 polymorphism was associated with arterial hypertension. However, the effects of the GNB3 825T allele on blood pressure were small and did not translate to a clinically relevant increase of risk for MI.