Background Different diagnostic criteria limit comparisons between populations in the prevalence of diastolic left ventricular (LV) dysfunction. We aimed to compare across populations age-specific echocardiographic criteria for diastolic LV dysfunction as well as their correlates and prevalence. Methods We measured the E and A peaks of transmitral blood flow by pulsed wave Doppler and the e' and a' peaks of mitral annular velocities by tissue Doppler imaging (TDI) in 2 cohorts randomly recruited in Belgium ( n = 782; 51.4% women; mean age, 51.1 years) and in Italy, Poland and Russia ( n = 476; 55.7%; 44.5 years). Results In stepwise regression, the multivariable-adjusted correlates of the transmitral and TDI diastolic indexes were similar in the 2 cohorts and included sex, age, body mass index, blood pressure and heart rate. Similarly, cut-off limits for the E/A ratio (2.5th percentile) and E/e' ratio (97.5th percentile) in 338 and 185 reference subjects free from cardiovascular risk factors respectively selected from both cohorts were consistent within 0.02 and 0.26 units (median across 5 age groups). The rounded 2.5th percentile of the E/A ratio decreased by ~0.10 per age decade in these apparently healthy subjects. The reference subsample provided age-specific cut-off limits for normal E/A and E/e' ratios. In the 2 cohorts combined, diastolic dysfunction groups 1 (impaired relaxation), 2 (possible elevated LV filling pressure) and 3 (elevated E/e' and abnormally low E/A) encompassed 114 (9.1%), 135 (10.7%), and 40 (3.2%) subjects, respectively. Conclusions The age-specific criteria for diastolic LV dysfunction were highly consistent across the study populations with an age-standardized prevalence of 22.4% vs. 25.1%.
Objective: The essential role of the renin-angiotensin-aldosterone system (RAAS) in controlling blood pressure has been well established. Genes encoding components of the RAAS have been proposed as candidate genes that determine genetic predisposition to hypertension and the risk of developing cardiovascular complications. The aim of the study was to evaluate follow-up changes in carotid intima-media thickness (IMT) in relation to genetic polymorphisms in 5 genes of the RAAS: angiotensin-converting enzyme (ACE I/D), angiotensinogen (AGT, A-6G), aldosterone synthase (CYP11B2, T-344C), angiotensin II receptors type 1 (ATR1, A1166C) and type 2 (ATR2, G1675A). Design and Methods: We examined 147 subjects, members of 45 nuclear families, enrolled in the population-based study in Krakow. The subjects underwent at baseline and on follow-up (6.4+/−0.5 yrs) conventional BP measurement during two separate visits, 5 times on each visit. Anthropometric data were collected with standardized protocol. Peripheral blood was sampled for genotyping. Carotid IMT was measured by carotid ultrasound (Hewlett Packard Sonos 2000 - baseline and VIVID 7 GE Pro - follow-up). In our analyses, we adjusted for covariables and non-independence among related subjects. Results: The study group included 71 M/76F, at baseline mean age was 37.6+/−14.2 yrs, BMI 26.0+/−5.2 kg/m2, BP 128.1+/−17.6/80.0+/−11.2 mmHg. In multivariate analyses, the change in IMT on follow-up was significantly associated with ACE I/D polymorphism (p = 0.008). The ACE II homozygotes showed higher increase in IMT as compared to D-allele carriers (change in IMT 0.252+/−0.043 vs. 0.093+/−0.022 mm, p = 0.002). The results were consistent among male and female, and among parents and offspring. The genetic polymorphisms in CYP11B2, AGT, ATR1 or ATR2 did not associate with phenotype under study. Conclusion: Insertion/deletion (I/D) polymorphism of the ACE gene associates with prospective increase in carotid intima-media thickness. However, the present findings need further confirmation in a larger/multicentre cohort.
Background: Control of hypertension (HT) in Polish general population is poor. However, achievement of treatment goal for hypertension is considered as a basis of secondary prevention of coronary heart disease (CAD). Methods: Consecutive patients in age <80 years hospitalized in years 2005–2006 due to acute coronary syndrome, PCI or CABG in Cracow province(1.2 mln. inhabitants) were included. Data for analysis were taken from subsamples examined in Euroaspire III- Poland (2006–2007). During the control visit, 6–18 months after hospitalization, blood pressure (BP) was measured twice and the rate of antihypertensive drugs was assessed. Treatment of HT among patients <65 and > = 65 years of age was compared. Results: There were 640 patients (455 men and 185 women) recruited in the hospital phase. Six - 18 month after hospitalization 513 patients were examined (80.1%). Systolic BP in patients <65 years of age (n = 305) was 133.8 ± 18.7 mmHg and among elderly patients (n = 208) 142.2 ± 21.9 mmHg (p < 0.05). Diastolic BP was found in both groups, respectively 85.5 ± 10.7 mmHg and 83.9 ± 11.6 mmHg (p = NS). Mean number of antihypertensive drugs in younger patients amount to 2.2 0.9, and in elderly patients 2.4 ± 0.9 (p < 0.05) (Table). Treatment target of BP (<140/90 mmHg or <130/80 mmHg in diabetic patients) was achieved in 44.4% younger patients and in 35.7% elderly. Conclusion: Although, combined antihypertensive treatment is commonly used, achievement of BP control is still insufficient, especially among patients with CAD > = 65 years of age.
Background: Although the differences between central and peripheral blood pressure (BP) values have been known for decades, the consequences of decision making based on peripheral rather than central BP have only recently been recognized. The predictive value of central systolic (SBP) and diastolic (DBP) pressure in coronary patients is unknown. Therefore, the aim of the present analysis was to compare predictive value of central systolic and diastolic pressure in patients undergoing non-emergency coronary angiography. Methods: The study group consisted of 852 patients (606 men and 246 women; mean age: 5.2 ± 10.0 years) with left ventricular ejection fraction >=50% undergoing coronary angiography. Invasive ascending aortic BP during catheterization was taken at baseline. A vast majority of participants was prescribed BP-lowering drugs. The duration of follow-up was 55.2 ± 17.3 months. The primary end point was defined as: cardiovascular death, myocardial infarction, stroke, cardiac arrest or myocardial revascularization. The Cox proportional hazard regression analysis was used to assess the relation between BP and primary end point. Results: During the follow-up the primary end point occurred in 169 (19.8%) patients. SBP, but not DBP was related to the risk of the primary endpoint (hazard ratio per one standard deviation increase [95% confidence intervals] 1.17 [1.01 – 1.36] and 0.92 [0.79 – 1.07] for SPB and DBP respectively). After multivariable adjustments once again SBP (1.17 [1.00 – 1.38]) but not DBP (0.92 [0.79 – 1.08]) was related to the prognosis. SBP was related to the prognosis in patients with DBP below the median value (1.36 [1.04 – 1.76]), but not in those with higher DBP at baseline (1.21 [0.93 – 1.58]). When SBP and DBP were forced together to the statistical model both occurred to be related to the primary end point (1.41 [1.15 – 1.72] and 0.75 [0.61 – 0.92]). Conclusions: Ascending aortic systolic, but not diastolic pressure is independently related to the risk of major cardiovascular events in patients undergoing coronary angiography.
The European guidelines for preventive cardiology give the highest priority to patients with established coronary artery disease. The aim of the analysis was to assess trend of blood pressure control in hypertensive subjects with coronary artery disease from 1997 to 2007. Methods: Consecutive patients hospitalized due to acute coronary syndrome or for myocardial revascularization procedures, below the age of < 71 years in five hospitals serving the area of the city of Krakow and surrounding districts inhabited by 1 200 000 population were identified and then followed up, interviewed and examined 6–18 months after discharge in 1997/1998, 1999/2000 and 2006/2007. Results: The number of hypertensives who participated in the surveys were: 229 in the first, 274 in the second and 346 in the third survey. The study groups differ in respect of mean age (57.2 ± 7.7 vs 58.7 ± 7.6 vs 59.4 ± 7.1 years; p < 0.01) but not in respect of sex distribution (men: 65% vs 66% vs 71%; p=NS) nor education. Proportion of uncontrolled blood pressure (BP >=140/90 mmHg) did not change from 1997/1998 to 1999/2000 (60% vs 61%; p=NS), but decreased in 2006/2007 (49%; p < 0.05 vs 1997/1998 and p < 0.01 vs 1999/2000). Mean systolic BP was lower in 2006/2007 (137.4 ± 20.7 mmHg) when compared with 1997/1998 (143.5 ± 22.4 mmHg; p < 0.001) and 1999/2000 (145.4 ± 21.8 mmHg; p < 0.001). Mean diastolic BP did not differ significantly (85.7 ± 10.8 mmHg vs 87.1 ± 12.0 mmHg vs 85.6 ± 11.2 mmHg; p=NS). The prescription rate of beta-blockers (68% vs 62% vs 89%; p < 0.001), ACE inhibitors/sartans (60% vs 61% vs 81%; p < 0.001), and diuretics (20% vs 27% vs 36%; p < 0.001) increased whereas prescription rate of calcium antagonists decreased (32% vs 39% vs 24%; p < 0.001). Conclusion: A significant improvement in the blood pressure control in coronary hypertensives could be observed in 2006/07.
Objectives: Central aortic blood pressure and aortic augmentation index (AI) are independent risk factor for cardiovascular events. Cross-sectional data confirms the relationship between family history of hypertension and parameters of structure and function of the large arteries in adult offspring. The objective of the present study was to assess differences in 5-years follow - up changes in BP parameters and AI in relation to parental history of hypertension. Methods: We recruited 201 members from random families (100 parent and 101 offspring (age at baseline: 58.5 and 28.9 years). From 75 normotensive descendants 9 were with a negative family history of hypertension, 36 with one hypertensive parents and 30 with both hypertensive parents. Initially and after follow up 4.8 ± 0.4 years we recorded the radial arterial waveform using the SphygmoCor device and evaluated peripheral AI (pAI) and central AI (cAI). Significance levels of between-group comparisons of the change from baseline were assessed by a general linear model that adjusted for baseline value and post-hoc Tukey test for multiple comparison. Results: In both groups with parental history of hypertension we observed significant increase in peripheral and central systolic blood pressure (SBP) during follow-up. We found higher increase in central SBP with lesser decrease in central diastolic BP in offspring with both hypertensive parents in comparison to participants with negative family history of hypertension (pTukey < 0.05). We observed significant elevation of brachial AI only in offspring with both hypertensive parents. Changes in central AI were more pronounced in both groups with parental history of hypertension, however this increase in cAI was higher in offspring with both hypertensive parents in comparison to those without hypertension in family (6.6 vs -3.0 (%); pTukey < 0.05). Conclusions: Parental history of hypertension enhances follow-up changes in BP and augmentation index. Our findings indicate that central parameters more effectively indicate differences in changes of systolic BP and arterial wall stiffening in relation to parental history of hypertension than brachial one.