A variant in the heart-specific fatty acid transport protein 6 is associated with lower fasting and postprandial TAG, blood pressure and left ventricular hypertrophy.

Fatty acid transport protein 6 (FATP6) is primarily expressed in the heart and seems to be involved in cardiac fatty acid uptake. Therefore, we investigated whether a variation in the 5'-untranslated region of the FATP6 gene is associated with features of the metabolic syndrome and signs of myocardial alteration or heart failure. A total of 755 male participants from a Metabolic Intervention Cohort Kiel were genotyped for the FATP6-7T>A polymorphism (rs2526246) and phenotyped for features of the metabolic syndrome. Participants underwent a glucose tolerance test and the postprandial assessment of metabolic variables after a standardised mixed meal. Left ventricular heart function was evaluated in fifty-four participants. Fasting (P = 0·01) and postprandial (P = 0·02) TAG concentrations were significantly lower in AA homozygotes when compared with wild-type carriers. Homozygosity of allele A was associated with significantly lower postprandial insulin concentrations after a glucose load and significantly lower systolic (P = 0·01) and diastolic (P = 0·01) blood pressure values compared with wild-type carriers. Accordingly, left ventricular heart mass was significantly lower in twenty-seven AA homozygotes in comparison with twenty-seven TT homozygotes, matched for BMI (P = 0·04). In conclusion, the effects of the FATP6 polymorphism on TAG are mediated by affluent dietary fat. The FATP6-7T>A polymorphism may protect from traits of the metabolic syndrome and CVD.

Evidence of pathological coronary flow patterns in patients with isolated coronary artery aneurysms.

OBJECTIVES: Aim of our study was to evaluate the coronary flow patterns and therapeutic effects of nitroglycerin (NTG) in patients with isolated large coronary artery aneurysms (CA). CA are defined as nonobstructive lesions of the epicardial coronary arteries with a luminal dilation >or=two-fold of the normal diameters. The pathophysiology of a potential coronary insufficiency in this entity is still unknown. METHODS: A coronary sinus study with incremental atrial pacing before and after the administration of 0.2 mg NTG was performed in 19 patients with bilateral large fusiform nonstenotic CA to evaluate an exercise-induced myocardial ischemia. The average peak velocity in the aneurysmatic segment of the proximal left anterior descending artery was simultaneously measured by a 14/1000 inch Doppler flow wire. The coronary flow volumes and vascular resistances were calculated. RESULTS: Evidence of exercise-induced myocardial ischemia was found in all patients presenting with a frank cardiac lactate production (10.2+/-3.3%) which was significantly aggravated by NTG (26.0+/-7.5%, P<0.003). 0.2 mg NTG provoked a long-lasting and significant decrease in coronary flow volume (from 140.2+/-34.2 to 91.2+/-21.8 ml/min, P<0.002), a marked increase in coronary vascular resistance (from 0.62 to 0.92 mmHG x ml/min(-1), P<0.002) and an inadequate increase in coronary flow volume under cardiac pacing. CONCLUSION: CA were identified as an entity of nonobstructive ischemic coronary artery disease with an exercise-induced myocardial ischemia and impaired flow volume. NTG exerted an adverse vasoactive effect in CA.

NT-proBNP is not elevated in patients with obstructive sleep apnoea.

BACKGROUND: N-terminal pro-brain natriuretic peptide (NT-ProBNP) has emerged as an important marker of cardiac stress and may reflect the severity of underlying cardiac dysfunction, which is thought to be associated with obstructive sleep apnoea syndrome (OSAS). METHODS: This study evaluated the plasma concentration of NT-ProBNP in 60 consecutive patients (median age 55.7 years, median body mass index (BMI) 31.8) who were referred to a sleep laboratory with a suspicion of OSAS. Each subject underwent measurement of morning NT-ProBNP plasma levels, polysomnography and echocardiography. Patients were treated with nasal continuous or bilevel positive airway pressure ventilation (nCPAP/BIPAP) or without mechanical respiratory support, depending on clinical symptoms and results of polysomnography. Three months after treatment of OSAS 28 of the patients were reassessed for re-evaluation of NT-ProBNP and polysomnography. RESULTS: Low or high levels of NT-proBNP were not associated with AHI and other sleep related indices (p>0.3). There was no correlation between NT-proBNP and AHI or other sleep related indices. In multiple regression analysis, NT-proBNP was significantly correlated with left ventricular ejection fraction, creatinine clearance and the presence of systemic arterial hypertension but not with AHI. CONCLUSIONS: Our results show by a robust multiple regression analysis, that NT-pro BNP is not associated with OSAS and NT-pro BNP cannot be used as a sensitive marker for underlying cardiovascular abnormalities in patients with OSAS.