Prevalence and covariates of abnormal left ventricular geometry in never-treated hypertensive patients in Tanzania.

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 (ß = 0.28), body mass index (ß = 0.20), peak early transmitral to medial mitral annulus velocity ratio (ß = 0.16), and with lower stress-corrected midwall shortening (scMWS) (ß = - 0.44) and estimated glomerular filtration rate (ß = - 0.16), all p < 0.05. Higher RWT was associated with higher systolic blood pressure (ß = 0.16), longer E-wave deceleration time (ß = 0.23) and lower scMWS (ß = - 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.

Determinants of systolic blood pressure response during exercise in overweight subjects.

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/m(2) 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/m(2) 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 (ß = 0.33), higher systolic ABP (ß = 0.22) and high-density lipoprotein (HDL)-cholesterol level (ß = 0.23, all p < 0.05) predicted higher systolic exercise BP independent of sex and peak oxygen uptake (multiple R(2) = 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.

Left atrial volume index as a marker of left ventricular diastolic dysfunction in asymptomatic Tanzanian diabetic patients.

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.

Global left ventricular load in asymptomatic aortic stenosis: covariates and prognostic implication (the SEAS trial).

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/m2. 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.

Hypertension in aortic stenosis: implications for left ventricular structure and cardiovascular events.

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.

Contrast stress echocardiography in hypertensive heart disease.

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.

Effect of obesity on left ventricular mass and systolic function in patients with asymptomatic aortic stenosis (a Simvastatin Ezetimibe in Aortic Stenosis [SEAS] substudy).

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.

Asymmetric septal hypertrophy - a marker of hypertension in aortic stenosis (a SEAS substudy).

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 > or =104 g/m(2) in women and > or =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.

Impact of hypertension on left ventricular structure in patients with asymptomatic aortic valve stenosis (a SEAS substudy).

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 >or=2.5 m/s and

Low-flow aortic stenosis in asymptomatic patients: valvular-arterial impedance and systolic function from the SEAS Substudy.

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).

Factors influencing left ventricular structure and stress-corrected systolic function in men and women with asymptomatic aortic valve stenosis (a SEAS Substudy).

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.