Electrocardiographic criteria which have the best prognostic significance in hypertensive patients with echocardiographic hypertrophy of left ventricle: 15-year prospective study.

BACKGROUND: Electrocardiography is the first-choice technique for detecting left ventricular hypertrophy in patients with arterial hypertension. It is necessary to know the probable outcome for every patient during the treatment, with the aim of improving cardiovascular event prevention. HYPOTHESIS: Certain electrocardiographic criteria for left ventricular hypertrophy may predict outcomes of patients with left ventricular hypertrophy during a 15-year follow-up. METHODS: Fifteen-year prospective study of 83 consecutive patients (53 male and 30 female; mean age 55.3 ± 8.1) with echocardiographic left ventricular hypertrophy (left ventricular mass index 170.3 ± 31.6 g/m2 ). Electrocardiographic left ventricular hypertrophy was determined by means of Gubner-Ungerleider voltage, Lewis voltage, voltage of R wave in aVL lead, Lyon-Sokolow voltage, Cornell voltage and Cornell product, voltage RV6 and RV5 ratio, Romhilt-Estes score, Framingham criterion and Perugia criterion. RESULTS: One or more composite events were registered in 32 (38.5%) patients during 15-year follow-up. Positive Lyon-Sokolow score (17.6% vs. 47.3%; P < 0.05), Lewis voltage (9.8% vs. 21.9%; P < 0.05), Cornell voltage (15.7% vs. 37.5%; P < 0.05), and Cornell product (9.8% vs. 34.4%; P < 0.01) were more frequent in a group of patients with composite events. Odd ratio for Cornell product was 4.819 (95% CI 1.486-15.627). CONCLUSION: Patients with echocardiographic left ventricular hypertrophy who had positive Lewis voltage, Lyon-Sokolow voltage, Cornell voltage, and Cornell product showed worse 15-year outcome. The strongest predictor of cardiovascular events was positive result of Cornell product.

Impact of metabolic syndrome on clinical severity and long-term prognosis in patients with myocardial infarction with ST-segment elevation.

AIMS: The aim of this study is to evaluate the impact of metabolic syndrome (MetS) on clinical severity and long-term prognosis in patients with myocardial infarction with ST-segment elevation (STEMI). METHODS: We examined 507 patients with STEMI, who were admitted for primary percutaneous coronary intervention classified according to the presence of MetS using American Heart Association and the National Heart, Lung, and Blood Institute definition. After applying these criteria, the patients were categorized into groups as patients with MetS and without MetS. We compared baseline characteristics, clinical findings, and outcomes between these groups. During the 48-month follow-up, we collected data about major adverse cardiac events (MACE) and mortality. RESULTS: The MetS group comprised 217 patients with MetS (mean age = 60.71 ± 11.52 years; 59 females), while the control group comprised 290 subjects (mean age = 57.50 ± 10.95 years; 54 females). The patients with and without MetS had similar parameters of clinical severity of STEMI but differed in severe coronary artery disease. During the follow-up period, a significantly higher percentage of myocardial infarction (6.91% vs 2.06%) and new revascularization (16.59% vs 8.97%) was recorded in the MetS group. On multivariate analysis, MetS was independently associated with MACE (HR = 1.834, 95% CI = 1.162-2.896, p = 0.009) but not with mortality (HR = 1.603, 95% CI = 0.864-2.973, p = 0.134). Among cardiovascular events that compose MACE, MetS was associated with new revascularization (HR = 2.204, 95% CI = 1.273-3.815, p=0.005). CONCLUSION: The presence of MetS in patients with STEMI is an independent risk factor for MACE, and this syndrome is strongly associated with new revascularization.

QTc dispersion and Cornell duration product can predict 10-year outcomes in hypertensive patients with left ventricular hypertrophy.

BACKGROUND: Persistent and adequate treatment of patients with arterial hypertension leads to more favorable disease outcome. HYPOTHESIS: Aside for the present left ventricular hypertrophy (LVH), there are other non-invasive parameters which can represent additional predictors of unfavorable prognosis in patients with essential arterial hypertension during the 10-year follow-up. METHODS: A hypertensive group with LVH (124 patients; age 57.0 ± 8.0; 84 males and 40 females) was included in the study and examined noninvasively. Patients used regular medication therapy during the follow-up period. RESULTS: During the 10-year follow-up period, unfavorable outcome was recorded for 40 (32.3%) patients. Patients with unfavorable outcome had higher baseline values of left ventricular mass index (178.9 ± 29.5 g/m2 vs 165.5 ± 29.5 g/m2 ; P < 0.05) and QTc dispersion (64.1 ± 24.7 ms vs 54.8 ± 19.4 ms; P < 0.05). Frequency of positive Cornell product was higher in the group of patients with unfavorable outcome (35% vs 22.2%; P < 0.01). Positive Lyon-Sokolow score did not show statistical significance (25% vs 11.9%; P = 0.06). Cornell product (ß = 0.234; P < 0.01) and QTc dispersion >65 ms (ß = 0.184; P < 0.05) had prognostic significance in LVH (multiple regression analysis: R = 0.314, R = 0.099, adjusted R = 0.084, standard error of the estimate = 0.449, P < 0.05). CONCLUSIONS: Patients with a positive Cornell product and larger QTc dispersion had more unfavorable 10-year outcomes compared with other patients with LVH.

Amlodipine as an antiischemic drug is superior to long acting nitrates.

European Society of Cardiology Guidelines cite results of meta-analysis that the use of calcium channel blockers results in fewer angina episodes per week vs. long-acting nitrates. Moreover, we listed 12 reasons more to prefer amlodipine over long-acting nitrates, especially in stable angina pectoris patients with arterial hypertension. It may be the way to decrease polypharmacy without loosing efficacy. Some important advantages of amlodipine versus long-acting nitrate(s) are: amlodipine also treats hypertension, it helps reducing hypertensive target organ damages (e.g. left ventricular hypertrophy) and prevents morning blood pressure surge. Moreover, amlodipine can be given once daily (which improves adherence), it produces neither tolerance nor rebound, it has less side effects.

[Effect of fosinopril on progression of the asymptomatic carotid atherosclerosis and left ventricular hypertrophy in hypertensive patients].

INTRODUCTION: The cardiovascular changes (vascular structure changes, hypertrophy of the left ventricle) contribute to both the increased cardiovascular morbidity and the mortality of essential hypertension. Therefore, modern treatment strategies should not only target blood pressure (BP) reduction but also normalize cardiovascular structure and function. OBJECTIVE: Aim of the study was to determine the effect of the ACE inhibitor Fosinopril on the intima-media thickness of the common carotid artery and on the left ventricle mass after 9-month treatment of hypertensive patients. METHOD: The study included 40 patients with the arterial hypertension and the left ventricle hypertrophy verified by echocardiography. The patients were randomized on A) ACE-inhibitor--Fosinopril and B) without ACE inhibitor--atenolol, and they were followed up 9 months. The groups were not different by age, sex, and metabolic status. Color Duplex ultrasonography of the carotid arteries was performed by Acuson Sequia C236 with high-frequency linear probe of 8 MHz. The intima-media thickness of the common carotids on the left and the right was measured in diastole at 1.5 cm from the highest point of bifurcation under maximal magnification. Using the same device, the left ventricle mass and other parameters of the left ventricle were determined in M-mode and by means of 2D image. RESULTS: After 9 months, BP in both groups was reduced in similar range (group A: systolic BP from 158 to 137 mmHg, and diastolic BP from 94 to 85 mmHg, and group B: systolic BP from 164 to 137 mmHg, and diastolic BP from 87 to 84 mmHg). The thickness of the intimomedial complex in patients using Fosinopril was decreased by 0.0278 +/- 0.03 mm, while in the group of patients that did not use the ACE-inhibitor, it was increased by 0.078 +/- 0.13 mm. The left ventricle mass in patients using Fosinopril was decreased by 5 grams (312 +/- 72 g vs. 307 +/- 77 g), while in group B patients, it was increased by 15 grams (323 +/- 79 g vs. 328 +/- 58 g. Diastolic function expressed through relation E/A was improved minimally in the group A, while it worsened by 0.1 in the group B. After 9 months, serious cardiovascular events were recorded (one infarction of myocardium and one hospitalization due to the unstable angina pectoris) in two patients of the group A, while four patients of the group B had serious CV events (1 cerebrovascular stroke and 3 hospitalizations due to unstable angina pectoris). CONCLUSION: The results of our study showed that the application of Fosinopril in patients with the arterial hypertension and the left ventricle hypertrophy could efficiently block further progression of the intima-medial thickness of the common carotid artery, reduce the left ventricle mass, and improve diastolic function of the left ventricle.