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Vittorio Palmieri

Publications and source records attributed to Vittorio Palmieri.

52 records · Page 3Linked to original sources
PubMed2003

Relation of left ventricular hypertrophy to inflammation and albuminuria in adults with type 2 diabetes: the strong heart study.

OBJECTIVE: To evaluate in adults with type 2 diabetes the extent to which the relation of left ventricular hypertrophy (LVH) to markers of systemic inflammation (fibrinogen and high-sensitivity C-reactive protein [hsCRP]) are affected by microangiopathy. RESEARCH DESIGN AND METHODS: We selected adults with type 2 diabetes using American Diabetes Association criteria from a population-based cohort, excluding those with medical history or electrocardiographic evidence of coronary heart disease or dialysis-dependent renal failure. LVH was assessed by echocardiogram. RESULTS: Of the 1299 eligible participants, 384 (29.6%) had LVH, which was associated with higher BMI, hsCRP, fibrinogen, and albuminuria in univariate analyses. After controlling for significant confounders, fibrinogen and albuminuria were higher in the presence of LVH (both P < 0.01), whereas hsCRP was not (P = 0.2), mostly because of the confounding effect of BMI. Adjustment for albuminuria abolished the relation of LVH to higher fibrinogen (P = 0.2). However, fibrinogen was significantly higher in participants with LVH among those without pathologic levels of albuminuria (<30 mg/g creatinuria), but not independent of BMI. Although hsCRP and fibrinogen were moderately correlated, fibrinogen, but not CRP, showed a significant relation with albuminuria. CONCLUSIONS: In adults with type 2 diabetes, echocardiographic LVH is associated with susceptibility to atherothrombosis and increased albuminuria, which is a marker of microangiopathy and endothelial dysfunction that appears in turn to be a relevant pathogenetic link between LVH and inflammation. However, in the absence of significant microalbuminuria, elevated BMI is a relevant pathogenetic factor in the relation of LVH to increased levels of markers of inflammation, potentially preceding development of significant albuminuria. In the presence of microangiopathy, we found that the atherothrombotic risk profile associated with LVH was independent of BMI and possibly reflected the association of LVH with a higher degree of endothelial dysfunction.

Aged↗
PubMed2002

Change in systolic left ventricular performance after 3 years of antihypertensive treatment: the Losartan Intervention for Endpoint (LIFE) Study.

BACKGROUND: We have shown that hypertensive patients with left ventricular (LV) hypertrophy have decreased LV midwall mechanics, but the effect of antihypertensive therapy remains unclear. METHODS AND RESULTS: Echocardiograms were recorded at baseline in 679 hypertensive patients and ECG LV hypertrophy and repeated yearly during 3 years of blinded treatment to achieve target blood pressures (BPs) of 140/90 mm Hg. On average, BP was reduced from 174+/-21 to 147+/-19 over 95+/-11 to 82+/-10 mm Hg and LV mass from 234+/-56 to 194+/-50 g. Endocardial fractional shortening (FS) decreased slightly, whereas midwall FS increased from 15.4+/-2.0% to 16.8+/-2.1% and stress-corrected midwall FS increased from 97+/-13 to 105+/-12% (all P<0.001). Change in midwall FS was related inversely to change in LV mass (LVM), relative wall thickness (RWT), and diastolic BP and directly to change in Doppler stroke volume (SV, all P<0.001). Multivariate analysis showed that change in MWS was independently inversely related to changes in LVM (beta=-0.211), RWT (beta=-0.334, all P<0.001), and diastolic BP (beta=-0.088, P<0.05) and directly related to SV (beta=0.192, P<0.001) with control for blinded therapy. Change in stress-corrected midwall shortening was inversely independently associated with changes in LVM (beta=-0.153) and RWT (beta=-0.562) and directly with changes in SV (beta=0.145) and systolic BP (beta=0.s221, all P<0.001) with control for blinded therapy. CONCLUSIONS: Antihypertensive therapy reduced LVM and increased LV midwall shortening and contractility with a small decrease in LV chamber function and significant increase in SV. Change in systolic LV performance was independently associated inversely with change in LVM, RWT, and BP and directly with change in SV.

Antihypertensive Agents↗
PubMed2002

Appetite suppressants and valvular heart disease in a population-based sample: the HyperGEN study.

PURPOSE: Previous studies of the association between the use of appetite suppressants and valvular heart disease have not accounted for the effects of valvular structure and aortic root diameter, which are associated with obesity. We assessed whether the use of the appetite suppressants fenfluramine/dexfenfluramine, either alone or with phentermine, was associated with aortic regurgitation while adjusting for these variables. SUBJECTS AND METHODS: The sample included 2524 adult participants in the population-based Hypertension Genetic Epidemiology Network study. Information regarding current drug use was assessed during a clinical examination. Medication use was continued at the time of echocardiographic study. Expert readers blinded to current therapy read echocardiograms centrally at Cornell Medical Center. Analyses of the associations between use of fenfluramine/dexfenfluramine (alone or with phentermine) and aortic regurgitation adjusted for potential confounders, including aortic root dilatation and valve fibrocalcification. RESULTS: Nineteen participants, all of whom had hypertension, were being treated with fenfluramine or dexfenfluramine (5 on these agents alone, 14 also with phentermine). Aortic regurgitation was present in 32% (n = 6) of those taking fenfluramine or dexfenfluramine versus 6% (162/2505) of remaining subjects (P = 0.001). In multivariate-adjusted analyses, treatment with fenfluramine or dexfenfluramine was associated with aortic regurgitation (odds ratio [OR] = 4.9; 95% confidence interval [CI]: 1.7 to 14) and aortic fibrocalcification (OR = 5.2; 95% CI: 1.9 to 15). CONCLUSION: In a population-based sample, use of fenfluramine or dexfenfluramine, alone or in combination with phentermine, was associated with aortic regurgitation independent of aortic dilatation or fibrocalcification.

Aortic Valve Insufficiency↗
PubMed2002

Gender difference in diastolic function in hypertension (the HyperGEN study).

Although several studies indicate that there are gender differences in left ventricular (LV) systolic function, it remains unclear whether similar differences exist with regard to diastolic function. Accordingly, Doppler echocardiograms were analyzed in 515 male and 839 female, mostly treated (95%) hypertensive participants enrolled in the Hypertension Genetic Epidemiology Network (HyperGEN) study with no evidence of abnormal wall motion or significant valvular heart disease. There was no difference in age between genders, but after adjusting for age and race, men had lower body mass indexes (29.8 +/- 5.2 vs 32.3 +/- 7.6 kg/m(2)) and heart rates (67 +/- 12 vs 69 +/- 11 beats/min) and higher systolic and diastolic blood pressures (BP) than women (134 +/- 20 vs 130 +/- 21 and 80 +/- 11 vs 72 +/- 11 mm Hg, all p <0.001). LV mass/height(2.7) was slightly greater in women than in men (43 +/- 10 vs 42 +/- 9 g/m(2.7), p <0.05). After adjusting for age, race, systolic BP, body mass index, heart rate, and LV hypertrophy, both mitral E-wave (70 +/- 18 vs 77 +/- 19) and A-wave (74 +/- 15 vs 79 +/- 17, both p <0.001) velocities were lower in men than in women, but the mitral E/A ratio and atrial filling fraction were nearly identical in both genders. Deceleration time (221 +/- 55 vs 214 +/- 46 cm/s, p = 0.018) and isovolumic relaxation time (IVRT) were longer in men than in women (85 +/- 18 vs 81 +/- 17 cm/s, p <0.001). Prolonged IVRT was present in more men than women (14% vs 7%, p <0.05). In analyses of covariance, adjusting for age, race, systolic BP, body mass index, heart rate, and medications, male gender remained related to prolonged deceleration time and IVRT. Thus, in this population-based sample of hypertensive adults, men had evidence of slower early diastolic LV filling than women. This gender difference in diastolic function may provide insight into gender differences in congestive heart failure and other specific cardiovascular diseases.

Age Distribution↗
PubMed2002

Mitral ratio of peak early to late diastolic filling velocity as a predictor of mortality in middle-aged and elderly adults: the Strong Heart Study.

BACKGROUND: With aging, left ventricular filling tends to decrease in early diastole, reducing the mitral ratio of peak early to late diastolic filling velocity (E/A). However, the prognostic significance of low or high E/A in older adults remains to be elucidated in population-based samples. METHODS AND RESULTS: Doppler echocardiograms were analyzed in 3008 American Indian participants in the second Strong Heart Study examination who had no more than mild mitral or aortic regurgitation. Participants were followed for a mean of 3 years after Doppler echocardiography to assess risks of all-cause and cardiac death associated with E/A <0.6 or >1.5; 2429 (81%) participants had normal E/A ratio, 490 (16%) had E/A <0.6, and 89 (3%) had E/A >1.5. All-cause mortality was higher with E/A <0.6 or E/A >1.5 (12% and 13% versus 6%), as was cardiac mortality (4.5% and 6.5% versus 1.6%; both P<0.001). Adjusting for age, sex, body mass index, systolic blood pressure, HDL and LDL cholesterol, smoking, hypertension, diabetes, coronary heart disease, left ventricular hypertrophy, and low ejection fraction (<40%), the relative risk of all-cause death with E/A >1.5 was 1.73 (95% CI, 0.99 to 3.03; P=0.05); the relative risk of cardiac death was 2.8 (95% CI, 1.19 to 6.75; P<0.05). E/A <0.6 was not independently associated with increased all-cause or cardiac mortality (P=0.19 and 0.31, respectively) after adjusting for covariates. CONCLUSIONS: In a population-based sample of middle-aged and elderly adults, mitral E/A >1.5 at baseline Doppler echocardiography is associated with 2-fold increased all-cause and 3-fold increased cardiac mortality independent of covariates; mitral E/A <0.6 was also associated with 2-fold increased all-cause and cardiac mortality but not independent of covariates.

Aged↗
PubMed2002

Change in diastolic left ventricular filling after one year of antihypertensive treatment: The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study.

BACKGROUND: It is well established that hypertensive patients with left ventricular (LV) hypertrophy have impaired diastolic filling. However, the impact of antihypertensive treatment and LV mass reduction on LV diastolic filling remains unclear. METHODS AND RESULTS: Echocardiograms were recorded in 728 hypertensive patients with ECG-verified LV hypertrophy (Cornell voltage-duration or Sokolow-Lyon) at baseline and after 1 year of blinded treatment with either losartan or atenolol-based regimen. Systolic and diastolic blood pressures (BP) were reduced on average 23/11 mm Hg; isovolumic relaxation time and E/A ratio became more normal, and LV inflow deceleration time prolonged (all P<0.001). Directionally opposite changes in isovolumic relaxation time (IVRT) and deceleration time indicate improvement in active LV relaxation and passive chamber stiffness during early diastole. Prevalences of normal LV filling increased, abnormal relaxation and pseudonormalization decreased, and restrictive filling pattern remained unchanged (P<0.05). Patients with reduction in LV mass had smaller left atrial diameter, shortened IVRT, increased E/A ratio, and prolonged LV inflow deceleration time (all P<0.001). Patients without LV mass reduction had no change in diastolic filling parameters (P=NS). IVRT shortening was independently associated with reduction in LV mass. Increase in E/A ratio was independently associated with reduction in diastolic BP, and increase in the deceleration time was independently associated with reduced end-systolic relative wall thickness. CONCLUSIONS: Antihypertensive therapy resulting in LV mass or relative wall thickness regression is associated with significant improvement of diastolic filling parameters related to active relaxation and passive chamber stiffness compared with patients without regression, independent of BP reduction; however, abnormalities of diastolic LV filling remain common.

Aged↗
PubMed2002

Correlates of left atrial size in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study.

Left ventricular hypertrophy has been suggested to mediate the relation between hypertension and left atrial enlargement, with associated risks of atrial fibrillation and stroke. However, less is known about correlates of left atrial size in hypertensive patients with left ventricular hypertrophy. We assessed left atrial size by echocardiography in 941 hypertensive patients, age 55 to 80 (mean, 66) years, with electrocardiographic left ventricular hypertrophy at baseline in the Losartan Intervention For Endpoint reduction in hypertension study. Enlarged left atrial diameter (women, >3.8 cm; men, >4.2 cm) was present in 56% of women and 38% of men (P<0.01). Compared with the 512 patients with normal left atrial size, the 429 patients with enlarged left atrium more often had mitral regurgitation, atrial fibrillation, and echocardiographic left ventricular hypertrophy. They also had higher age, systolic blood pressure, pulse pressure, weight, body mass index, left ventricular internal chamber dimension, stroke volume, and mass and lower relative wall thickness and ejection fraction (all, P<0.05). In logistic regression analysis, left atrial enlargement was related to left ventricular hypertrophy and eccentric geometry; greater body mass index, systolic blood pressure, and age; female gender; mitral regurgitation; and atrial fibrillation (all, P<0.05). Thus, left atrial size in hypertensive patients with electrocardiographic left ventricular hypertrophy is influenced by gender, age, obesity, systolic blood pressure, and left ventricular geometry independently of left ventricular mass and presence of mitral regurgitation or atrial fibrillation.

Aged↗
PubMed2002

Correlates of pulse pressure reduction during antihypertensive treatment (losartan or atenolol) in hypertensive patients with electrocardiographic left ventricular hypertrophy (the LIFE study).

In hypertensive patients, pulse pressure has been related to hypertension-induced target organ damage and risk of cardiovascular events. However, correlates of pulse pressure reduction during antihypertensive treatment have been less extensively investigated. We related pulse pressure changes to clinical and echocardiographic findings before and after 2 years of antihypertensive treatment in 767 patients aged 55 to 80 years (mean 66) in the Losartan Intervention For End point reduction in hypertension study. Over 2 years, blood pressure and pulse pressure were reduced from 173/98 to 147/84 mm Hg and from 75 to 63 mm Hg, respectively, both p <0.001. In linear multivariate analysis controlling for initial pulse pressure, 2-year reduction in pulse pressure correlated negatively with age and concomitant diabetes mellitus, and positively with body height and 2-year reduction in mean blood pressure (multiple R(2) = 0.42, p <0.01). When dividing the study population into 2 groups using a prognostically validated partition for pulse pressure, patients with pulse pressure > or =63 mm Hg after 2 years of antihypertensive treatment (n = 349) were older and shorter, included more women and patients with isolated systolic hypertension, diabetes mellitus, albuminuria, and echocardiographic left ventricular hypertrophy at baseline, and also had a smaller decrease in mean blood pressure and the urinary albumin/creatinine ratio over 2 years (all p <0.05). Thus, in hypertensive patients with electrocardiographic left ventricular hypertrophy, older age, less reduction in mean blood pressure, concomitant diabetes mellitus, and shorter stature are associated with attenuated pulse pressure reduction during antihypertensive treatment.

Aged↗
PubMed2002

Relation of insulin to left ventricular geometry and function in African American and white hypertensive adults: the HyperGEN study.

BACKGROUND: It has been suggested that the trophic effects of insulin may contribute to left ventricular (LV) hypertrophy in hypertension, but few population-based data exist to assess the potential impact of insulin level on LV structure or systolic function. METHODS: Fasting plasma insulin levels (log-transformed) in 1,542 nondiabetic African American or white hypertensive participants in the Hypertension Genetic Epidemiology Network (HyperGEN) study were compared to indices of LV geometry and function, with adjustment for potential confounders (age, sex, ethnicity, blood pressure (BP), body mass index, height and antihypertensive drugs). RESULTS: In simple correlation analysis, a weak positive relation (r = 0.078, P =.002) was found between LV mass and insulin, principally due to positive correlations (r = 0.22 and 0.50) of both variables to body mass index. Multivariate analysis, adjusting for age, sex, ethnicity, body size, systolic BP, and antihypertensive drugs revealed a modest negative relation between insulin and LV mass (r = -0.08, P =.001) due to a negative relationship between insulin with LV chamber size (r = - 0.10, P <.001) and no significant relation to LV wall thicknesses. These results were confirmed in additional analysis controlling for a positive relation (r =.19, P <.0001) of insulin to heart rate, and the relation with insulin became slightly more negative when LV mass was indexed for height(2.7) (r = -0.13, P <.001). After adjustment for covariates, there were no significant relations of insulin to LV ejection fraction or stress-corrected midwall shortening; however, insulin was negatively related to stroke volume (r = -0.12, p < 0.001) and was weakly related positively to relative wall thickness (r =.053) (P =.04). CONCLUSIONS: After adjustment for body mass index and other covariates, insulin in nondiabetic hypertensive individuals has weak negative relations to LV chamber size, mass, and stroke volume, and also has weak positive relations to relative wall thickness but not to measures of LV systolic function. Thus, native plasma insulin level may not play a major independent role in the pathogenesis of hypertensive LV hypertrophy or dysfunction.

Adult↗
PubMed2002

Urine albumin/creatinine ratio and echocardiographic left ventricular structure and function in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE study. Losartan Intervention for Endpoint Reduction.

BACKGROUND: Albuminuria, reflecting systemic microvascular damage, and left ventricular (LV) geometric abnormalities have both been shown to predict increased cardiovascular morbidity and mortality. However, the relationship between these markers of cardiovascular damage has not been evaluated in a large hypertensive population. METHODS: The urine albumin/creatinine ratio (UACR) and echocardiographic measures of LV structure and function were obtained in 833 patients with stage I to III hypertension and LV hypertrophy determined by electrocardiogram (ECG) (Cornell voltage-duration or Sokolow-Lyon voltage criteria) after 14 days of placebo treatment. RESULTS: Patients' mean ages were 66 years, 42% were women, 23% had microalbuminuria, and 5% had macroalbuminuria. Patients with eccentric or concentric LV hypertrophy had higher prevalences of microalbuminuria (average 26%-30% vs 9%, P <.001) and macroalbuminuria (6%-7% vs <1%, P <.001). Furthermore, patients with microalbuminuria and macroalbuminuria had a significantly higher LV mass and lower endocardial and midwall fractional shortening. Patients with abnormal diastolic LV filling parameters had a significantly increased prevalence of microalbuminuria. In univariate analyses, UACR correlated positively to LV mass, systolic blood pressure, age (all P <.001) and pulse pressure/stroke volume and negatively to relative wall thickness (both P <.01) and endocardial (P <.05) and midwall shortening (P <.001) but not to diastolic filling parameters. In multiple regression analysis higher UACR was associated with higher LV mass (beta=.169, P <.001) independently of older age (beta =.095, P <.01), higher systolic pressure (beta=.163), black race (beta=.186), and diabetes (beta=.241, all P <.001). CONCLUSIONS: In hypertensive patients with ECG LV hypertrophy, abnormal LV geometry and high LV mass are associated with high UACR independent of age, systolic blood pressure, diabetes, and race, suggesting parallel cardiac and microvascular damage.

Aged↗
PubMed2002

Association of left ventricular hypertrophy with metabolic risk factors: the HyperGEN study.

OBJECTIVE: To determine whether combinations of metabolic risk factors (obesity, diabetes and hypercholesterolemia) influence the magnitude of left ventricular (LV) mass and prevalence of LV hypertrophy. DESIGN: Cross-sectional, relational. METHODS: A total of 1627 hypertensive (85.9% treated, 1036 women, 1041 African Americans) and 342 normotensive (180 women, 183 African Americans) participants in the Hypertension Genetic Epidemiology Network (HyperGEN) Study, without prevalent cardiovascular disease, were studied. Echocardiographic LV mass, normalized by height(2.7) or fat-free mass or body surface area (BSA) and the ratio of stroke volume to pulse pressure as a percentage of predicted (as a crude estimate of arterial compliance) were analyzed in relation to obesity [by body mass index (BMI)], central fat distribution (by waist circumference), diabetes (by ADA criteria) and hypercholesterolemia. RESULTS: Obesity, hypercholesterolemia, and diabetes were more frequent among hypertensives than normotensives (all P < 0.001). After controlling for age, sex, race and type and combination of antihypertensive medication, LV mass/height(2.7), but not LV mass/fat-free mass and LV mass/BSA, increased with the number of metabolic risk factors, both in normotensive and hypertensive participants, also after further adjustment for blood pressure (all P < 0.001). Stroke volume/pulse pressure also decreased in hypertensive, but much less in normotensive subjects, with increasing number of metabolic risk factors, independently of relevant confounders (P < 0.0001). Prevalence of LV hypertrophy was predicted by older age, hypertension, central fat distribution, black race and independently increased with the number of associated metabolic risk factors (P < 0.0001). CONCLUSIONS: The progressive addition of metabolic risk factors including central obesity, diabetes and hypercholesterolemia is associated with higher LV mass normalized by height(2.7), independently of hypertension and other important biological covariates. Obesity played a major role in this association. This finding indicates that LV mass is a potentially useful bioassay of strategies of global cardiovascular prevention.

Adipose Tissue↗
PubMed2002

Relations of pulse pressure and other components of blood pressure to preclinical echocardiographic abnormalities.

OBJECTIVE: To evaluate the extent to which pulse pressure (PP) is associated with echocardiographic abnormalities, and in particular to whether PP is related to LV hypertrophy taking into account other blood pressure (BP) components. DESIGN: Cross-sectional. SETTING: University hospital, hypertension outpatient unit. PARTICIPANTS: A total of 275 adults (mean age 47 years, range 19-69, 3% aged > or = 65) with essential hypertension. Overt coronary artery disease, valvular disease and secondary hypertension were exclusion criteria. Subjects were divided in two groups with PP < or = 50 or PP > 50 mmHg. OUTCOME MEASURES: Left ventricular (LV) mass, hypertrophy, LV systolic dysfunction. RESULTS: Prevalence of LV hypertrophy was higher in subjects with clinic PP > 50 mmHg. Subjects with PP > 50 mmHg had higher clinic and ambulatory systolic than subjects with PP < or = 50 mmHg while diastolic BP did not differ between groups. PP and systolic BP, either clinic or ambulatory, showed similar correlation to LV hypertrophy in separate logistic multivariate models. Using different methodologies, PP was not related to LV mass index or hypertrophy when the effect of its component systolic BP was taken into account. In separate analyses, PP was not significantly related to ejection fraction or midwall mechanics. CONCLUSION: Middle-aged clinically healthy hypertensives with PP > 50 mmHg had two-fold higher prevalence of LV hypertrophy than those with PP < or = 50 mmHg, which may contribute to the higher cardiovascular risk in subjects with higher PP. However, in our sample, PP was not related to LV hypertrophy independently of systolic BP, suggesting that systolic BP is the explanatory link of the relation between PP and LV hypertrophy.

Adult↗
PubMed2002

Progressive hypertrophy regression with sustained pressure reduction in hypertension: the Losartan Intervention For Endpoint Reduction study.

OBJECTIVE: To examine the time course of left ventricular (LV) geometric response to blood pressure (BP) control during 2 years of systematic antihypertensive treatment. DESIGN: A total of 754 hypertensive patients with left ventricular hypertrophy (LVH) by Cornell voltage-duration product or Sokolow-Lyon voltage criteria on a screening electrocardiogram had their LV mass measured by echocardiogram at enrolment in the Losartan Intervention For Endpoint Reduction (LIFE) trial, and after 12 and 24 months of blinded therapy with losartan-based or atenolol-based regimens. SETTING: The LIFE trial, in which hypertensive patients with electrocardiographic LVH (Cornell voltage-duration product > 2440 mm x ms and/or Sokolow-Lyon voltage criteria SV1 + RV5-6 > 38 mm) were randomized to >or= 4 years double-blinded treatment with losartan or atenolol. PARTICIPANTS: A total of 754 LIFE participants with serial echocardiographic measurements of LV geometry. INTERVENTIONS: None. MAIN OUTCOME MEASURES: LV wall thicknesses, diameter and mass, and its indices. RESULTS: Mean systolic/diastolic BP fell from 173/95 to 150/84 mmHg after 1 year (P < 0.001) and to 148/83 mmHg at year 2 (P = not significant). Mean echocardiographic LV mass fell from 233 g at baseline to 206 g after 1 year (P < 0.001, adjusted for change in systolic BP) and to 195 g at year 2 (P < 0.001 versus year 1), with a parallel decrease in indexed LV mass [from 56.1 to 49.7 g/m2.7 (P < 0.001), to 47.1 g/m2.7 (P < 0.001 versus year 1)]. Relative wall thickness decreased from 0.41 at baseline to 0.37 at year 1 (P < 0.001), to 0.36 at year 2 (P < 0.001 versus year 1). As a result, there were serial decreases in prevalences of eccentric LVH [44 to 38%, and to 30% (P < 0.001 versus year 1)] and concentric LVH [24 to 7% (P < 0.001), to 2% (P < 0.05 versus year 1)], and increases in the proportion with normal LV geometry [22 to 50% (P < 0.001), and to 64% (P < 0.01 versus year 1)]. CONCLUSIONS: Sustained BP reduction in hypertensive patients with target organ damage causes continued decrease in echocardiographic LV mass and prevalence of anatomic LVH for at least 2 years despite only small BP decreases after the first year of blinded therapy. These data document cardiac benefit of sustained BP control and suggest that maximum LVH regression with effective antihypertensive treatment requires at least 2 years.

Aged↗
PubMed2002

Left ventricular hypertrophy in hypertension as a predictor of coronary events: relation to geometry.

The present review examines epidemiological evidence for a relation of left ventricular hypertrophy with coronary heart disease, and mechanisms that may represent pathophysiological links between left ventricular hypertrophy and coronary events. Left ventricular hypertrophy has been demonstrated to be a powerful predictor of coronary heart disease, and when geometry is concentric the relation is even stronger. In addition to its association with risk factors for atherosclerosis and mechanisms that precipitate acute heart attacks, left ventricular hypertrophy also directly predisposes to and aggravates clinical presentation of coronary heart disease through a number of biological mechanisms. These include the following: increase in oxygen requirement related to left ventricular geometry; coronary hypertension, with endothelial dysfunction and reduced coronary reserve; diastolic dysfunction; and structural remodelling of myocardium and vascular bed. Some of these alterations are also worsened by underlying coronary heart disease, and can potentially be maintained by loop mechanisms. A recognizable stage of abnormal coronary haemodynamics in the context of left ventricular hypertrophy is probably that at which coronary reserve is impaired in the absence of any other sign of heart disease; in many circumstances, this may occur early in the disease process.

Coronary Disease↗
PubMed2002

[Echocardiographic evaluation of ventricular hypertrophy].

Quantitative echocardiography is the gold standard for the evaluation of abnormalities in left ventricular (LV) geometry and systolic function, information very important for risk stratification, and also applicable in clinical practice when some conditions are met. Few primary measures (LV diameter, septal and posterior wall thickness) provide a valuable information which fully represents the type and degree of hemodynamic alteration. These measures should be collected ideally by M-mode tracings, but often M-mode examination cannot be performed. When M-mode is suboptimal, LV mass can be computed using two-dimensional imaging and the formulas used for M-mode. LV mass is expressed as an index normalized for some measure of body size. Normalization for height in meters to the power 2.7 can identify a higher proportion of individuals at high cardiovascular risk and provides a greater attributable risk than other methods of indexation. When LV hypertrophy develops to provide sufficient strength to compensate for hemodynamic overload, the increase in LV mass is not clearly associated with increased cardiovascular risk. In contrast, individuals with LV mass inappropriately high as compared to the value sufficient to compensate for hemodynamic load at a given body size present with a phenotype characterized by high cardiovascular risk, even in the absence of arterial hypertension.

Echocardiography↗