Search PubMed⌕ Search

Biomedical subjects

Peter Bogaty

Publications and source records attributed to Peter Bogaty.

25 records · Page 2Linked to original sources
PubMed2002

Association of fibrinogen and lipoprotein(a) as a coronary heart disease risk factor in men (The Quebec Cardiovascular Study).

Fibrinogen has been prospectively found to correlate with coronary heart disease (CHD) but a similar association has not been well established for lipoprotein (a) (Lp(a)). Plasma lipids, Lp(a), and fibrinogen levels were measured in 2,125 men (aged 47 to 76 years) who were free of clinical CHD. During a 5-year follow-up period, 116 first CHD events were documented. Men with CHD were older, smoked more, had a higher prevalence of diabetes, and higher levels of systolic blood pressure, cholesterol, low-density lipoprotein cholesterol, Lp(a), and fibrinogen, and lower plasma high-density lipoprotein cholesterol levels. Only fibrinogen levels in the upper tertile of the distribution compared with the lower tertiles were associated with a significant risk of CHD (adjusted risk ratio 2.5; 95% confidence interval [CI] 1.4 to 4.2; p = 0.0010). Such an association was not observed with Lp(a). To assess a possible relation between fibrinogen and Lp(a) to the risk of CHD events, men were assigned to 1 of 4 groups according to fibrinogen median levels and a Lp(a) cut-off level of 300 mg/L: group 1: fibrinogen < 4.05 g/L and Lp(a) < 300 mg/L; group 2: fibrinogen < 4.05 g/L and Lp(a) > or =300 mg/L; group 3: fibrinogen > or =4.05 g/L and Lp(a) < 300 mg/L; and group 4: fibrinogen > or =4.05 g/L and Lp(a) > or =300 mg/L. Using group 1 as a reference, a significant risk ratio was only documented in group 4 (2.5; 95% CI 1.2 to 5.1; p = 0.0132). In this population, high fibrinogen levels associated with high Lp(a) levels significantly increased the risk of CHD.

Adult↗
PubMed2002

Is anteroseptal myocardial infarction an appropriate term?

Anteroseptal myocardial infarction is defined by the presence of electrocardiographic Q-waves limited to precordial leads V(1) to V(2), V(3), or V(4). We sought to determine whether this term is appropriate by correlating electrocardiographic, echocardiographic, and angiographic findings. We studied 50 consecutive patients admitted for a first acute myocardial infarction with Q-waves in precordial leads V(1) to V(2)-V(4), and who had undergone echocardiography and coronary angiography during hospitalization. Echocardiograms in the apical long-axis, two-chamber, and four-chamber views were studied using a wall motion scoring index.Q-waves were present in precordial leads V(1)-V(2) in 4 patients, V(1)-V(3) in 28 patients, and V(1)-V(4) in the remaining 18 patients. The presumptive culprit lesion was in the proximal segment of the left anterior descending artery in 15 patients, in the middle segment in 33 patients, and indeterminate in 2 patients. This lesion was before the first septal branch in 19 patients and after the first septal branch in 29. Mean (+/- SD) left ventricular ejection fraction was 51% +/- 10%. Echocardiographic analysis showed that the septal wall was never the only wall that was affected. However, the apex was affected in all patients and was the only wall that was affected in 26 (52%) patients (apical wall index, 2.1 +/- 0.5). In the remaining 24 patients, the septum was also affected (septal index, 1.5 +/- 0.3), but less severely than was the apex (apical index, 2.3 +/- 0.4; P <0.0001 vs. septum). In these 24 patients, the anterior and lateral walls were also affected (anterior index, 1.4 +/- 0.4; lateral index, 1.1 +/- 0.2), but again, less severely than was the apex (P <0.0001 for both vs. apex). Neither angiographic nor echocardiographic data support the notion of an isolated anteroseptal myocardial infarction. Left anterior descending artery involvement appears more often to be midsegment and postseptal. The apex is always and principally affected. These findings suggest that anteroseptal myocardial infarction is a misnomer and that the V(1) to V(2)-V(4) Q-wave pattern should be considered to indicate a predominantly apical, and generally limited, myocardial infarction.

Electrocardiography↗
PubMedDate not supplied

Does hormonal status influence the clinical presentation of acute coronary syndromes in women?

BACKGROUND: Previous studies suggest that the clinical presentation of acute coronary syndromes (ACS) may differ between women and men. It is not known if different clinical presentations may be explained by hormonal status in women with ACS. Our objective was to compare the clinical presentation of ACS between premenopausal (PRE) women and post-menopausal women with hormone replacement therapy (HRT) and without (POST). METHODS: This was a prospective study of consecutive women admitted with a diagnosis of ACS (myocardial infarction [MI] or unstable angina). All women answered a detailed questionnaire that included a list of 27 clinical symptoms. Symptom results were adjusted for age and current coronary event diagnosis. RESULTS: Seventy-three Caucasian women were studied. No differences were found in terms of the frequency of reported typical symptoms of ACS between PRE (n = 23), HRT (n = 32), and POST (n = 18). However, PRE more often reported atypical chest symptoms than HRT and POST women (57% vs. 31% vs. 22%, PRE vs. HRT vs. POST, respectively, p = 0.05). HRT and POST women experienced substernal chest pain more frequently than PRE (44% vs. 78% vs. 83%, p = 0.03). In contrast, PRE more frequently tended to experience chest pressure (57% vs. 31% vs. 39%, p = 0.2) or chest pain in other locations (22% vs. 3% vs. 6%, p = 0.06). HRT and POST groups reported more frequent indigestion-like pain/discomfort (22% vs. 50% vs. 56%, p = 0.04) and midback pain (35% vs. 63% vs. 72%, p = 0.04) during ACS compared with PRE women. POST experienced sudden fatigue more frequently than PRE and HRT (61% vs. 53% vs. 89%, p = 0.03). CONCLUSIONS: Our results suggest that almost all women admitted with ACS experienced typical chest symptoms but frequently reported both typical and atypical symptoms. Independently of age, atypical chest symptoms occurred more frequently in premenopausal women than in postmenopausal women with or without HRT.

Adult↗
PubMedDate not supplied

The ACE-DD genotype is associated with endothelial dysfunction in postmenopausal women.

OBJECTIVE: To evaluate the effects of the angiotensin-converting enzyme (ACE) insertion/deletion (I/D), the angiotensinogen M235T and the angiotensin II type 1 receptor A1166C polymorphisms, and hormone therapy used on endothelial function in postmenopausal women without manifestation of coronary artery disease. DESIGN: Sixty-four postmenopausal women (42 hormone therapy users and 22 hormone therapy nonusers) without clinical manifestation of coronary artery disease were evaluated using external vascular ultrasonography to measure endothelium-dependent (hyperemic response, flow-mediated dilatation) and -independent (nitroglycerin) dilatation. Genotypes were determined by polymerase chain reaction amplification. RESULTS: Women with the ACE-DD genotype displayed a lower flow-mediated dilatation compared to those with the ACE-II genotype (8.4% +/- 3.9% vs 12.6% +/- 5.4%, P = 0.04). Endothelial function was not associated with the angiotensinogen M235T and anglotensin II type 1 receptor A1166C polymorphisms. ACE polymorphism seems to modulate endothelial function among postmenopausal women without hormone therapy (8.2% +/- 5.1% vs 18.4% +/- 5.9% for the DD and the II genotype, respectively, P = 0.02). However, in hormone therapy users, flow-mediated dilatation was similar according to the ACE genotypes. CONCLUSIONS: Our findings suggest that ACE-I/D polymorphism is related to endothelial dysfunction in postmenopausal women. Furthermore, a potential interaction between estrogen users and ACE polymorphism on endothelial function may be present.

Alleles↗