Genetic research has elucidated molecular mechanisms of heart failure (HF). Peroxisome proliferator-activated receptors (PPARs) seem to be important in etiology of HF. The aim of study was to find the correlation between PPARγ expression during development of HF in patients and coronary artery disease (CAD) after coronary artery bypass-grafting (CABG). Methods and Results. We followed up 157 patients (mean age 63) with CAD without clinical, laboratory, or echo parameters of HF who underwent CABG. Clinical and laboratory status were assessed before CABG and at 1, 12, and 24 months. During CABG slices of aorta (Ao) and LV were collected for genetic research. HF was defined as LVEF <40% or NT-proBNP >400 pg/mL or 6MWT <400 m. Patients were divided into 2 groups: with and without HF. PPARγ expression in Ao and LV was not increased in both groups at 2-year follow-up. Sensitivity of PPARγ expression in Ao above 1.1075 in detection of HF was 20.5% (AUC 0.531, 95% CI 0.442–0.619). Positive predictive value (Ppv) was 85.7%. Sensitivity and specificity of PPARγ expression in the LV in detection of HF were 58% and 92.9%, respectively (AUC 0.540, 95% CI 0.452–0.626). Ppv was 73.2%. Conclusion. PPARγ expression in Ao and LV was comparable and should not be used as predictive factor for development of HF in patients with CAD after CABG.
Mild left ventricular hypertrophy (LVH) has been considered as one of the possible structural, physiological adaptations to regular, intensive physical activity. However, it may also appear as one of the subclinical complications of hypertension. In athletes, the differential diagnosis between these two entities may be complicated as regular physical activity may potentially mask the presence of arterial hypertension. We sought to determine the relation between LVH in middle-age athletes and the presence of hypertension. The study included 71 healthy, male long-time amateur athletes (mean age 41 ± 6 years, 83% endurance and 17% power sports) without known hypertension or any other cardiovascular diseases and with normal self-measured and office blood pressure. All subjects underwent resting electrocardiogram, transthoracic echocardiography, maximal exercise test on a treadmill and ambulatory blood pressure monitoring. LVH was diagnosed as left ventricular wall diameter >11 mm. Hypertension was defined as mean 24 h systolic blood pressure (SBP) ≥ 130 mmHg and/or diastolic blood pressure (DBP) ≥ 80 mmHg. Exaggerated blood pressure response (EBPR) to exercise was defined as SBP ≥ 210 mmHg. LVH (range > 11 to 14 mm) was found in 20 subjects (28%) and hypertension was diagnosed in 33 subjects (46%). Athletes with LVH were more likely to have hypertension than those without LVH (70% vs. 37%, p = 0.01). EBPR to exercise was found equally common in athletes with and without LVH (35% vs. 29%, p = 0.68), but more often in subjects with hypertension (51% vs. 13%, p < 0.001). Presence of LVH and hypertension was equally common in the studied endurance and power sport athletes (p = 0.66 and p = 0.79, respectively). In comparison to athletes without LVH, those with LVH had larger left atrial size (26 ± 6 vs. 21 ± 4 cm2, p < 0.001) and a tendency for lower left ventricular diastolic function (E/A 1.2 ± 0.4 vs. 1.5 ± 0.4, p = 0.05) and a larger ascending aorta diameter (34 ± 3 vs. 32 ± 3, p = 0.05), but a similar left ventricular end-diastolic diameter (51 ± 3 vs. 51 ± 4, p = 0.71). The presence of mild left ventricular hypertrophy in middle-age male amateur athletes with normal home and office blood pressure may be considered as a potential sign of masked hypertension. It should not be overlooked as an element of a physiological adaptation to exercise and may warrant further medical evaluation with ambulatory blood pressure monitoring.
Surgical aortic valve replacement (AVR) still remains the treatment of choice in symptomatic significant aortic stenosis (AS). Due to technical problems, extensive calcification of the ascending aorta (“porcelain aorta”) is an additional risk factor for surgery and transapical aortic valve implantation (TAAVI) is likely to be the only rescue procedure for this group of patients. We describe the case of an 81-year-old woman with severe AS and “porcelain aorta”, in whom the only available life-saving intervention was TAAVI.
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