Background: Persistence or development of Cornell product left ventricular hypertrophy (LVH) is associated with increased heart failure (HF) risk that is partly explained by greater LV systolic dysfunction. However, whether new or persistent Cornell product LVH during antihypertensive treatment is associated with worse LV diastolic function is unclear.
Methods: Left ventricular diastolic function was examined in relation to year-3 ECG LVH in 377 hypertensive patients with a preserved LV ejection fraction (>45%) at year-3. Cornell product >2440 mm·ms defined ECG LVH.
Results: In multivariate models adjusting for age, sex, change from baseline to year-3 systolic blood pressure, and baseline and change from baseline to year-3 Sokolow-Lyon voltage, persistent or new Cornell product LVH at year-3 remained associated with year-3 abnormal half filling time (OR 1.63, 95% CI 1.04-2.55 p = 0.034), with a trend toward higher odds of abnormal third filling time (OR 1.51, 95% CI 0.087 p = 0.087) and total filling time (OR 1.79, CI 0.98-3.27 p = 0.059).
Conclusion: In hypertensive patients undergoing antihypertensive therapy, persistence or development of Cornell product ECG LVH at year-3 follow-up is modestly associated with LV diastolic dysfunction. These findings suggest that diastolic dysfunction may be a mechanism via which changing ECG LVH influences HF risk.
Introduction: Exercise echocardiography is a reliable routine test in patients with known or suspected coronary artery disease. However, in ∼15% of all patients, stress echocardiography leads to false-positive stress echocardiography results. We aimed to investigate the impact of hypertension on stress echocardiographic results.
Methods: We performed a retrospective study of patients with suspected or known stable coronary artery disease who underwent a bicycle exercise stress echocardiography. Patients with false-positive stress results were compared with those with appropriate results.
Results: 126 patients with suspected or known coronary artery disease were included in this retrospective study. 23 patients showed false-positive stress echocardiography results. Beside comparable age, gender distribution and coronary artery status, hypertension was more prevalent in patients with false-positive stress results (95.7% vs. 67.0%, p = 0.0410). Exercise peak load revealed a borderline-significance with lower loads in patients with false-positive results (100.0 (IQR 75.0/137.5) vs. 125.0 (100.0/150.0) W, p = 0.0601). Patients with false-positive stress results showed higher systolic (2.05 ± 0.69 vs. 1.67 ± 0.39 mmHg/W, p = 0.0193) and diastolic (1.03 ± 0.38 vs. 0.80 ± 0.28 mmHg/W, p = 0.0165) peak blood pressure (BP) per wattage. In a multivariate logistic regression test, hypertension (OR 17.6 [CI 95% 1.9-162.2], p = 0.0115), and systolic (OR 4.12 [1.56-10.89], p = 0.00430) and diastolic (OR 13.74 [2.46-76.83], p = 0.00285) peak BP per wattage, were associated with false-positive exercise results. ROC analysis for systolic and diastolic peak BP levels per wattage showed optimal cut-off values of 1.935mmHg/W and 0.823mmHg/W, indicating false-positive exercise echocardiographic results with AUCs of 0.660 and 0.664, respectively.
Conclusions: Hypertension is a risk factor for false-positive stress exercise echocardiographic results in patients with known or suspected coronary artery disease. Presence of hypertension was associated with 17.6-fold elevated risk of false-positive results.
Reducing salt intake is a factor related to life style which can influence the prevention of blood pressure. This study was conducted to assess the impact of social class on the amount of salt intake in patients with hypertension in Iran. This was an observational on the intake of salt, as estimated by Kawasaki formula in a sample from Iranian population, stratified for social background characteristics. The finding in general was that the estimated salt intake was somewhat higher in subjects from a lower social background, while the opposite was true for lipid levels (LDL and HDL cholesterol). There was also a significant correlation between salt intake and the level of systolic blood pressure, but not the level of diastolic blood pressure. Considering high salt intake (almost double the standard amount in Iran), especially in patients with low-social class and the effects of salt on human health, it is suggested to design and perform suitable educational programs based on theories and models of health education in order to reduce salt intake.
Background: It has been demonstrated that circulating endothelial progenitor cells (EPCs) number reflects the endogenous vascular repair ability, with the EPCs pool declining in presence of cardiovascular risk factors. Several drugs, including dihydropyridine calcium channel blockers, have been reported to elicit antioxidant and anti-inflammatory properties, as well as to improve vascular remodeling and dysfunction. However, no data are available about the effects of lercanidipine on EPCs. The aim of the present study was therefore to investigate the effects of short-term treatment with lercanidipine on circulating EPCs, as well as on indices of inflammation and oxidative stress.
Patients and methods: Twenty essential hypertensive patients were included in the study and treated for 4 weeks with lercanidipine 20 mg per day orally. Investigations were performed in basal condition, after appropriate wash out of previous treatments, and after 4 weeks of lercanidipine treatment. Inflammatory and oxidative stress markers were assessed by ELISA technique. Lin-/7AAD-/CD34+/CD133+/VEGFR-2 + and Lin-/7AAD-/CD34+/VEGFR-2 + cells were identified by flow cytometry and considered as EPCs. EPCs cells were expressed as number of cells per million Lin-mononuclear cells.
Results: Circulating EPCs were significantly increased after lercanidipine treatment (CD34+/CD133+/VEGFR-2 + cells: 78.3 ± 64.5 vs 46.6 ± 32.8; CD34+/VEGFR-2+: 87996 ± 165116 vs 1026 ± 1559, respectively, p < 0.05). A modest reduction in circulating indices of inflammation was also observed.
Conclusions: In conclusion, lercanidipine is able to increase the number of circulating EPCs, possibly through a reduction of low-grade inflammation.