AIM. To assess prevalence, type and covariates of abnormal left ventricular (LV) geometry in untreated native Tanzanian patients with hypertension in relation to normotensive controls. METHODS. Echocardiography was performed in 161 untreated hypertensive outpatients and 80 normotensive controls at a tertiary hospital in Tanzania. Hypertensive heart disease was defined as presence of increased LV mass or relative wall thickness (RWT). RESULTS. The prevalence of hypertensive heart disease increased with the severity of hypertension and was on average 62.1% among patients and 12.5% in controls. In multivariate analyses, higher LV mass index was associated with higher systolic blood pressure (β = 0.28), body mass index (β = 0.20), peak early transmitral to medial mitral annulus velocity ratio (β = 0.16), and with lower stress-corrected midwall shortening (scMWS) (β = - 0.44) and estimated glomerular filtration rate (β = - 0.16), all p < 0.05. Higher RWT was associated with higher systolic blood pressure (β = 0.16), longer E-wave deceleration time (β = 0.23) and lower scMWS (β = - 0.66), irrespective of LV mass (all p < 0.05). CONCLUSION. Subclinical hypertensive heart disease is highly prevalent in untreated native hypertensive Tanzanians and associated with both systolic and diastolic LV dysfunction. Management of hypertension in Africans should include high focus on subclinical hypertensive heart disease.

Abstract Aim. Higher systolic exercise blood pressure (BP) is associated with increased cardiovascular risk in hypertension. We aimed at identifying covariates of systolic exercise BP in overweight subjects. Methods. 77 subjects with body mass index (BMI) > 27 kg/m2 and without known heart disease were tested. BP was measured by sphygmomanometry before and at all exercise stages during maximal exercise capacity testing on a treadmill. High peak systolic exercise BP was defined as ≥ 200 mmHg. Results. The study population was 48 ± 10 years and included 60% women and 42% with known hypertension. Average BMI was 32.6 ± 4.8 kg/m2 and clinic BP 132/82 ± 17/8 mmHg. High systolic exercise BP was found in 32%. Subjects with high systolic exercise BP had higher systolic clinic and 24-h ambulatory BP (ABP), as well as lower peak oxygen uptake, compared with subjects with normal systolic exercise BP (all p < 0.05). In multiple regression analysis known hypertension (β = 0.33), higher systolic ABP (β = 0.22) and high-density lipoprotein (HDL)-cholesterol level (β = 0.23, all p < 0.05) predicted higher systolic exercise BP independent of sex and peak oxygen uptake (multiple R2 = 0.32, p < 0.001). Conclusion. Among overweight subjects, known hypertension, higher systolic ABP and HDL-cholesterol level were the most important factors predicting higher systolic exercise BP.

Introduction Valvuloarterial impedance (Zva) is a measure of global (combined valvular and arterial) load opposing left ventricular (LV) ejection in aortic stenosis (AS). The present study identified covariates and tested the prognostic significance of global LV load in patients with asymptomatic AS. Methods 1418 patients with mild-moderate, asymptomatic AS in the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) study were followed for a mean of 43±14 months during randomized, placebo-controlled treatment with combined simvastatin 40 mg and ezetimibe 10 mg daily. High global LV load was defined as Zva >5 mm Hg/ml/m 2 . The impact of baseline global LV load on rate of major cardiovascular (CV) events, aortic valve events and total mortality was assessed in Cox regression models reporting hazard ratio (HR) and 95% Confidence Intervals (CI). Results High global LV load was found in 18% (n=252) of patients and associated with female gender, higher age, hypertension, more severe AS and lower ejection fraction (all p<0.05). A total of 476 major CV events, 444 aortic valve events and 132 deaths occurred during follow-up. In multivariate Cox regression analyses, high global LV load predicted higher rate of major CV events (HR 1.35 [95% CI 1.08-1.71], P=0.010) and aortic valve events (HR 1.41 [95% CI 1.12-1.79], P=0.004) independent of hypertension, LV ejection fraction, female gender, age, abnormal LV geometry and AS severity, but failed to predict mortality. Conclusion In asymptomatic AS, assessment of global LV load adds complementary information on prognosis to that provided by hypertension or established prognosticators like AS severity and LV ejection fraction.

The impact of hypertension on left ventricular structure and outcome during progression of aortic valve stenosis has not been reported from a large prospective study. Data from 1616 patients with asymptomatic aortic stenosis randomized to placebo-controlled treatment with combined simvastatin and ezetimibe in the Simvastatin Ezetimibe in Aortic Stenosis Study were used. The primary study end point included combined cardiovascular death, aortic valve events, and ischemic cardiovascular events. Hypertension was defined as history of hypertension or elevated baseline blood pressure. Left ventricular hypertrophy was defined as left ventricular mass/height(2.7) ≥ 46.7 g/m(2.7) in women and ≥ 49.2 g/m(2.7) in men and concentric geometry as relative wall thickness ≥ 0.43. Baseline peak aortic jet velocity and aortic stenosis progression rate did not differ between hypertensive (n = 1340) and normotensive (n = 276) patients. During 4.3 years of follow-up, the prevalence of concentric left ventricular hypertrophy increased 3 times in both groups. Hypertension predicted 51% higher incidence of abnormal LV geometry at final study visit independent of other confounders (P<0.01). In time-varying Cox regression, hypertension did not predict increased rate of the primary study end point. However, hypertension was associated with a 56% higher rate of ischemic cardiovascular events and a 2-fold increased mortality (both P<0.01), independent of aortic stenosis severity, abnormal left ventricular geometry, in-treatment systolic blood pressure, and randomized study treatment. No impact on aortic valve replacement was found. In conclusion, among patients with initial asymptomatic mild-to-moderate aortic stenosis, hypertension was associated with more abnormal left ventricular structure and increased cardiovascular morbidity and mortality.

Aim: To determine the prevalence of left atrial (LA) enlargement and its relation to left ventricular (LV) diastolic dysfunction among asymptomatic diabetic outpatients attending Muhimbili National Hospital in Dar es Salaam, Tanzania. Methods: Echocardiography was performed in 122 type 2 and 58 type 1 diabetic patients. Diastolic dysfunction was defined as peak transmitral blood velocity to medial mitral annulus velocity (E/E') ratio >= 15. LA volume indexed to body surface area (LAVI) was considered enlarged if >= 29 ml/m(2). Results: Enlarged LAVI and LV diastolic dysfunction were more common in type 2 than in type 1 diabetic patients (44.3 vs 25.9% and 20.5 vs 3.5%, respectively, both p < 0.05). In multivariate linear regression analysis, larger LAVI was associated with LV diastolic dysfunction independent of significant associations with LV mass index and presence of mitral regurgitation in type 2 diabetic patients, while LV mass index, lower ejection fraction and longer duration of diabetes were the main covariates of larger LAVI in type 1 diabetic patients (all p < 0.05). Conclusion: Enlarged LA is common among asymptomatic Tanzanian diabetic patients, and particularly associated with LV diastolic dysfunction in type 2, and with cardiomyopathy and lower systolic function in type 1 diabetic patients.

The impact of hypertension on left ventricular structure and outcome during progression of aortic valve stenosis has not been reported from a large prospective study. Data from 1616 patients with asymptomatic aortic stenosis randomized to placebo-controlled treatment with combined simvastatin and ezetimibe in the Simvastatin Ezetimibe in Aortic Stenosis Study were used. The primary study end point included combined cardiovascular death, aortic valve events, and ischemic cardiovascular events. Hypertension was defined as history of hypertension or elevated baseline blood pressure. Left ventricular hypertrophy was defined as left ventricular mass/height 2.7 ≥46.7 g/m 2.7 in women and ≥49.2 g/m 2.7 in men and concentric geometry as relative wall thickness ≥0.43. Baseline peak aortic jet velocity and aortic stenosis progression rate did not differ between hypertensive (n=1340) and normotensive (n=276) patients. During 4.3 years of follow-up, the prevalence of concentric left ventricular hypertrophy increased 3 times in both groups. Hypertension predicted 51% higher incidence of abnormal LV geometry at final study visit independent of other confounders ( P <0.01). In time-varying Cox regression, hypertension did not predict increased rate of the primary study end point. However, hypertension was associated with a 56% higher rate of ischemic cardiovascular events and a 2-fold increased mortality (both P <0.01), independent of aortic stenosis severity, abnormal left ventricular geometry, in-treatment systolic blood pressure, and randomized study treatment. No impact on aortic valve replacement was found. In conclusion, among patients with initial asymptomatic mild-to-moderate aortic stenosis, hypertension was associated with more abnormal left ventricular structure and increased cardiovascular morbidity and mortality.

Hypertension is associated with atherosclerosis and cardiac and vascular structural and functional changes. Myocardial ischemia may arise in hypertension independent of coronary artery disease through an interaction between several pathophysiological mechanisms, including left ventricular hypertrophy, increased arterial stiffness and reduced coronary flow reserve associated with microvascular disease and endothelial dysfunction. The present case report demonstrates how contrast stress echocardiography can be used to diagnose myocardial ischemia in a hypertensive patient with angina pectoris but without significant obstructive coronary artery disease. The myocardial ischemia was due to severe resistant hypertension complicated with concentric left ventricular hypertrophy and increased arterial stiffness.

Obesity and hypertension are associated with left ventricular (LV) hypertrophy. Whether an increased body mass index (BMI) affects LV hypertrophy in patients with asymptomatic aortic stenosis independent of hypertension is not known. We used the clinical blood pressure, BMI, and echocardiographic findings recorded at baseline of 1,703 patients with asymptomatic aortic stenosis (AS) participating in the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) study. The patient population was divided into 3 BMI classes: normal BMI, 18.5 to 24.9 kg/m(2); overweight, BMI 25.0 to 29.9 kg/m(2); and obese, BMI > or =30.0 kg/m(2). For the total study population, the average blood pressure was 145/82 +/- 20/10 mm Hg, age 67 +/- 10 years, BMI 26.9 +/- 4.3 kg/m(2), and peak transaortic velocity 3.1 +/- 0.5 m/s. The prevalence of hypertension increased with increasing BMI class (43% vs 51% and 63%, p <0.01). The LV mass and prevalence of LV hypertrophy increased with an increasing BMI (22% in normal, 38% in overweight, and 54% in obese patients). The LV ejection fraction and stress-corrected mid-wall fractional shortening decreased (p <0.01 vs normal-weight group). On multiple logistic regression analysis, the presence of LV hypertrophy was associated with a greater BMI (odds ratio 1.15, 95% confidence interval 1.12 to 1.18), independent of a history of hypertension, the severity of AS, older age, systolic blood pressure, and lower LV ejection fraction (all p <0.05). Valve regurgitation and gender had no independent association with the presence of LV hypertrophy. In conclusion, a greater BMI was associated with the presence of LV hypertrophy in patients with asymptomatic AS, independent of AS severity and the presence of hypertension.

Objective Both hypertension and aortic valve stenosis induce left ventricular hypertrophy. However, less is known about the influence of concomitant hypertension on left ventricular structure in patients with aortic valve stenosis.Methods Baseline Doppler echocardiography was performed in 1720 patients with asymptomatic aortic valve stenosis (peak transaortic velocity >= 2.5 m/s and <= 4.0 m/s) recruited in the Simvastatin and Ezetimibe in Aortic Stenosis study at 173 centers in seven European countries. Patients were grouped as normotensive (n = 482) or hypertensive (n = 1238) according to history of hypertension or clinic blood pressure greater than 140 mmHg systolic or greater than 90 mmHg diastolic at baseline visits.Results Hypertensive patients were older, more obese, and included more women (all P<0.05). Furthermore, the hypertensive group had higher wall thicknesses and left ventricular mass and higher prevalence of left ventricular hypertrophy (40 vs. 25%) and increased relative wall thickness (21 vs. 14%, both P<0.01). On the basis of aortic valve area and energy loss the degree of aortic valve stenosis did not differ between the groups. In multivariate analysis, hypertension predicted higher left ventricular mass independent of other well known confounders including male sex, circumferential end-systolic stress, body mass index, aortic regurgitation, left ventricular ejection fraction and severity of aortic stenosis (multiple R-2 = 0.30, P<0.001).Conclusion In patients with asymptomatic aortic stenosis, concomitant hypertension significantly influences left ventricular geometry and is associated with higher left ventricular mass, relative wall thickness and higher prevalence of left ventricular hypertrophy. J Hypertens 28: 377-383 (C) 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.

Background. Some patients with aortic stenosis develop asymmetric septal hypertrophy ( ASH) that may influence the surgical approach and is associated with higher perioperative morbidity. The aim of this analysis was to characterize further this subtype of aortic stenosis patients. Methods. Baseline data in 1719 patients with asymptomatic aortic stenosis, participating in the Simvastatin Ezetimibe in Aortic Stenosis study evaluating the effect of combined treatment with simvastatin and ezetimibe on progression of aortic stenosis was used. The study population was divided according to presence of ASH ( interventricular septal/posterior wall thickness ratio >1.5). Left ventricular (LV) hypertrophy was considered present if LV mass index >= 10(4) g/m(2) in women and >= 116 g/m(2) in men. Results. ASH was present in 22% of patients and associated with higher LV mass index, total peripheral resistance and peak transaortic velocity and concomitant hypertension ( all p<0.05). Thirty-four percent of patients with ASH had combined ASH and LV hypertrophy ( asymmetric LV hypertrophy). These patients had higher systolic blood pressure, lower LV ejection fraction and larger left atrial diameter than patients with ASH only. In logistic regression analyses, hypertension was the most important predictor both for ASH ( odds ratio, OR 1.38 [1.05-1.82]) and for asymmetric LV hypertrophy (OR 2.99 [1.71-5.25]), both p<0.05) independent of other covariates including severity of aortic stenosis. Conclusion. Hypertension is the main clinic characteristic of ASH and asymmetric LV hypertrophy in patients with asymptomatic aortic stenosis independent of severity of aortic stenosis.

BACKGROUND:Pulse pressure (PP) has been related to risk of cardiovascular events in hypertension. However, less is known about modification of this risk marker during antihypertensive treatment in patients with left ventricular (LV) hypertrophy.METHODS:Associations of in-treatment PP with LV systolic function and cardiovascular events was assessed in 883 patients with electrocardiographic LV hypertrophy during 4.8 years of randomized losartan- or atenolol-based treatment within the echocardiographic substudy of the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study.RESULTS:PP was similarly reduced by both treatments. In different multiple regression models, lower in-treatment PP was independently associated with lower in-treatment LV ejection fraction (beta=0.16), stress-corrected midwall shortening (beta=0.20), stroke volume (beta=0.11) and cardiac index (beta=0.07, all p<0.05). In time-varying Cox regression models, 10 mmHg lower in-treatment PP was associated with a 28% higher rate of cardiovascular events [hazard ratio, HR = 1.28 (1.09 - 1.52), p<0.01] independent of in-treatment LV mass and ejection fraction, history of ischemic heart disease, Framingham risk score and study treatment allocation.CONCLUSION:During systematic antihypertensive treatment in hypertensive patients with electrocardiographic LV hypertrophy, lower in-treatment PP was associated with lower in-treatment LV function and cardiac output as well as higher rate of cardiovascular events.

OBJECTIVES This study sought to assess the impact of valvuloarterial impedance on left ventricular (LV) myocardial systolic function in asymptomatic aortic valve stenosis (AS).BACKGROUND In atherosclerotic AS, LV global load consists of combined valvular and arterial resistance to LV ejection. Global load significantly impacts LV ejection fraction (EF) in symptomatic AS, but less is known about its effect on LV myocardial function in asymptomatic AS.METHODS Echocardiograms in 1,591 patients with asymptomatic AS (67 +/- 10 years, 51% hypertensive) at baseline in the SEAS (Simvastatin Ezetimibe in Aortic Stenosis) study evaluating placebo-controlled combined simvastatin and ezetimibe treatment in AS were used to assess LV global load as valvuloarterial impedance and LV myocardial function as stress-corrected midwall shortening. The study population was divided into tertiles of global load. Stress-corrected midwall shortening was considered low if <87% in men and <90% in women. Low-flow AS was defined as stroke volume index <22 ml/m(2.04).RESULTS Energy loss index decreased (0.85 cm(2)/m(2) vs. 0.77 and 0.75 cm(2)/m(2)) and the prevalence of low stress-corrected midwall shortening increased (10% vs. 26% and 63%) with increasing LV global load (all p < 0.001). The EF was low in only 2% of patients. Patients with low-flow AS had higher LV global load and more often low midwall shortening than those with normal-flow AS (9.66 +/- 2.23 mm Hg/ml.m(2.04) and 77%, vs. 6.38 +/- 2.04 mm Hg/ml.m(2.04) and 30%, respectively, p < 0.001). In logistic regression analysis, LV global load was a main predictor of low stress-corrected midwall shortening independent of male sex, concentric LV geometry, LV hypertrophy (all p < 0.001), concomitant hypertension, and aortic regurgitation.CONCLUSIONS LV global load impacts LV myocardial function in asymptomatic AS independent of other main covariates of LV systolic function. LV myocardial systolic dysfunction is common in asymptomatic AS in particular in patients with low-flow AS and increased valvuloarterial afterload, whereas EF is generally preserved. (An Investigational Drug on Clinical Outcomes in Patients With Aortic Stenosis [Narrowing of the Major Blood Vessel of the Heart]; NCT00092677) (J Am Coll Cardiol Img 2009;2:390-9) (C) 2009 by the American College of Cardiology Foundation

To identify determinants of left ventricular (LV) structure and stress-corrected systolic function in men and women with asymptomatic aortic stenosis (AS), Doppler echocardiography was performed at baseline in 1,046 men and 674 women 28 to 86 years of age (mean 67 +/- 10) recruited in the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) study evaluating placebo-controlled combined simvastatin and ezetimibe treatment in AS. LV hypertrophy was less prevalent in women despite older age, higher systolic blood pressure, and smaller aortic valve area/body surface area (all p values <0.05). In logistic regression analyses, LV hypertrophy was independently associated with male gender, severity of AS, hypertension, higher systolic blood pressure, and lower stress-corrected midwall shortening (scMWS) or stress-corrected fractional shortening (scFS; all p values <0.01). In men aortic regurgitation also was a predictor of LV hypertrophy (p <0.05). Women had greater scFS and scMWS when corrected for LV size or geometry (all p values <0.001). In multivariate analyses, female gender predicted 11% greater scFS and 4% greater scMWS independent of age, body mass index, heart rate, aortic valve area, LV mass, relative wall thickness, aortic regurgitation, hypertension, and end-systolic stress (R(2) = 0.23 and 0.59, respectively, p <0.001). In conclusion, the major determinants of LV hypertrophy in patients with asymptomatic AS are male gender, severity of AS, and concomitant hypertension. Women have higher stress-corrected indexes of systolic function independent of LV geometry or size, wall stress, older age, or more concomitant hypertension.

in men/women), RWT and midwall shortening were evaluated in 1728 patients (39% women, aged 67±10 years) with asymptomatic AS, re- cruited in the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) study. RWT was defined as the ratio of either posterior wall thickness (RWTp, concentric geometry if ≥0.43), or the average of posterior and septal wall thickness (RWTm, concentric geometry if ≥0.45) to LV radius. Both variables were also normalized for age using previously published regression coefficients (RWTpa and RWTma, concentric geometry if ≥0.40 and 0.41, respectively). Results: Average peak transaortic velocity was 3.09±0.54 m/sec. Compared to RWTp and RWTm, use of RWTpa and RWTma reclassified LV geometry in 2.8% and 3.5% of patients (Table 1). Compared to RWTp, use of RWTm reclassified LV geometry in 11.2% of patients (183 from eccentric to concen- tric and 11 from concentric to eccentric geometry) (p<0.01). Compared to those who maintained eccentric or concentric geometry, respectively, pa- tients reclassified to concentric geometry by RWTm included more hyper- tensive patients, had larger LV mass and wall thicknesses and lower midwall shortening (all p<0.05), while patients reclassified to eccentric geometry did not differ in clinical characteristics, but had lower LV septal thickness and higher midwall shortening (both p<0.01). Conclusions: Use of age-normalized RWT modestly reclassified LV geom- etry in this elderly population. However, in patients with asymptomatic AS, defining RWT from average septal and posterior wall thickness compared to posterior wall thickness alone, considerably increased both prevalence of concentric geometry and associated midwall dysfunction. ), with low gradient-low EF (LVEF £35%, GDT £30 mm Hg) and who had aortic valvular replacement (AVR) were prospectively enrolled. Preoperative contractile reserve (CR) during dobutamine infusion was defined by an increase in stroke volume of ≥20% compared with baseline values. CR was present in 35 patients (Group I, 76%) and absent in 11 patients (Group II, 24%). In the overall sample, operative mortality was 17%. Operative mortality was 8.5% in group I compared with 45% in group II (p=0.013). In univariate analysis, lack of CR (p=0.013), three-vessel coronary artery disease (p=0.02) and GDT £20 mm Hg (p=0.02) were associated with operative mortality. In- dependent predictors of operative mortality were GDT £20 mmHg (odds ra- tio=11; 95% CI, 1.2 to 107.6; p=0.03), lack of contractile reserve (odds ratio =10; 95% CI, 1.2 to 81.6; p=0.034) and three vessels coronary artery disease (odds ratio =11; 95% CI, 1.2 to 107.6; p=0.034). All patients without CR and with GDT £20 mmHg (n=3) died in the perioperative period. Conclusions: These data further support in patients with low GDT-low EF AS the value of very low gradient (±20 mm Hg) at rest and of CR on DSH for preoperative risk stratification. Patients with GDT £20 mm Hg and lack of CR have an extremely high operative mortality.