Left Ventricular Hypertrophy In Hypertensive Subjects Research Articles

Hypersensitive C-reactive protein as a potential indicator for predicting left ventricular hypertrophy in elderly community-dwelling patients with hypertension

BackgroundThe aim of this study was to investigate the relationship between Hypersensitive C-reactive protein (hs-CRP) and left ventricular hypertrophy (LVH) in elderly community-dwelling patients with hypertension.MethodsA cross-sectional study was conducted, involving the recruitment of 365 elderly hypertensive residents ≥ 65 years of age from five communities. The participants were divided into two groups: an LVH group (n = 134) and a non-LVH group (n = 231), based on the left ventricular mass index (LVMI) determined by echocardiography. Spearman correlation analysis was used to assess the relationship between hs-CRP and LVH. Univariate and Multivariate analysis was performed to detect variables associated with LVH. The diagnostic value of hs-CRP for LVH was expressed as the area under the receiver operating characteristic (ROC) curve.ResultsThe incidence of LVH in elderly hypertension patients in the community was 36.7%. The hs-CRP levels were significantly higher in subjects with LVH compared to those without LVH (1.9 [0.8, 2.9] vs. 0.7 [0.4, 1.4], P = 0.002). Spearman correlation analysis demonstrated a positive correlation between hs-CRP and LVMI (r = 0.246, P < 0.001), as well as with IVST (r = 0.225, P < 0.001) and LVPWT (r = 0.172, P = 0.001). Among elderly hypertensive residents in the community, the cut-off value of hs-CRP for diagnosing LVH was 1.25 mg/L (sensitivity: 57.5%; specificity: 78.4%), and the area under the ROC curve for hs-CRP to predict LVH was 0.710 (95%CI: 0.654–0.766; P < 0.001). In the final model, hs-CRP ≥ 1.25 mg/L (OR = 3.569; 95%CI, 2.153–5.916; P<0.001) emerged as an independent risk factor for LVH. This association remained significant even after adjusting for various confounding factors (adjusted OR = 3.964; 95%CI, 2.323–6.765; P < 0.001).ConclusionsThis community-based cohort of elderly hypertensive individuals demonstrates a strong association between hs-CRP levels and the presence of LVH. The hs-CRP ≥ 1.25 mg/L may serve as an independent predictor for LVH in hypertensive subjects and exhibit good diagnostic efficacy for LVH.

Clinical perspectives on the adoption of the artificial intelligence-enabled electrocardiogram

To determine normal limits for major ECG variables, and the electrocardiographic impact of hypertension, in a rural sub-Saharan African setting.This cross-sectional study included adults aged ≥25 years from Tanvè Health Study (TAHES) cohort. ECG were recorded at rest at 25 mm/s using a standard 12‑lead device. Wave amplitudes and durations were measured. Corrected QT interval (QTc) was calculated using Bazett's formula. Sokolow-Lyon, Cornell and Peguero-Lo Presti criteria were determined to assess left ventricular hypertrophy (LVH).ECG was recorded among 997 out of 1407 TAHES participants. After exclusion of subjects with hypertension or diabetes, normal limits, defined as the 2nd and 98th percentiles, were evaluated in 622 healthy participants (median: 37 years; 60.1% women). The following limits were established in men (women): heart rate: 50 to 100 (55 to 102) beats/min, P wave duration: 80 to 120 (80 to 120) ms, PR interval: 120 to 200 (120 to 200) ms, QTc: 315 to 470 (323 to 465) ms, QRS duration: 50 to 120 (50 to 110) ms. Upper limits (in millimeter) for the Sokolow-Lyon, Cornell and Peguero-Lo Presti for men (women) were 47 (38), 30 (22) and 39 (30), respectively, all above current reference limits. The prevalence of LVH in hypertensive subjects according to these criteria were lower than those estimated according to current LVH criteria.The normal limits of ECG variables determined in this African population differ from those in Caucasians, indicating that ethnicity must be considered in ECG interpretation.

Normal limits of electrocardiogram in Africans and their consequences on the prevalence of left ventricular hypertrophy in hypertensive individuals: Insights from the TAHES study

AimsTo determine normal limits for major ECG variables, and the electrocardiographic impact of hypertension, in a rural sub-Saharan African setting. MethodsThis cross-sectional study included adults aged ≥25 years from Tanvè Health Study (TAHES) cohort. ECG were recorded at rest at 25 mm/s using a standard 12‑lead device. Wave amplitudes and durations were measured. Corrected QT interval (QTc) was calculated using Bazett's formula. Sokolow-Lyon, Cornell and Peguero-Lo Presti criteria were determined to assess left ventricular hypertrophy (LVH). ResultsECG was recorded among 997 out of 1407 TAHES participants. After exclusion of subjects with hypertension or diabetes, normal limits, defined as the 2nd and 98th percentiles, were evaluated in 622 healthy participants (median: 37 years; 60.1% women). The following limits were established in men (women): heart rate: 50 to 100 (55 to 102) beats/min, P wave duration: 80 to 120 (80 to 120) ms, PR interval: 120 to 200 (120 to 200) ms, QTc: 315 to 470 (323 to 465) ms, QRS duration: 50 to 120 (50 to 110) ms. Upper limits (in millimeter) for the Sokolow-Lyon, Cornell and Peguero-Lo Presti for men (women) were 47 (38), 30 (22) and 39 (30), respectively, all above current reference limits. The prevalence of LVH in hypertensive subjects according to these criteria were lower than those estimated according to current LVH criteria. ConclusionThe normal limits of ECG variables determined in this African population differ from those in Caucasians, indicating that ethnicity must be considered in ECG interpretation.

Factors Contributing to Development and Reversal of LVH: A Pilot Study.

Left Ventricular Hypertrophy (LVH) often reflects as a physiological adaptation to chronic pressure overload. It has been identified as a strong independent risk factor of all-cause mortality and adverse cardiac events. Since not all subjects with hypertension develop LVH, understanding the clinical factors contributing to the development of LVH and the appropriate diagnostic and treatment strategies may help clinicians in conducting more definitive evaluation and managing the disease effectively. To assess the incidence of LVH in hypertensive subjects and the factors influencing its development and reversal. The study also evaluated the most effective diagnostic technique and therapy that could improve the disease symptoms and prognosis. The prospective study, conducted at Jagadguru Sri Shivarathreeshwara (JSS) Medical College JSS University, Mysore, India, included 50 patients with hypertension. Detailed history of the recruited subjects was collected from patient records and through physical examination. Demographic and clinical characteristics such as age, gender, BMI, and stage of hypertension (stage I HTN and stage II HTN) were also obtained. Funduscopic examination was done for all patients for evidence of hypertensive retinopathy. Echocardiography (ECHO), electrocardiography (ECG), and chest X-Ray were used for detection of LVH. The patients were reviewed after six months and reassessment of LVH was carried out. Statistical analysis was conducted using SPSS software and R 3.2 package. Angiotensin-Converting Enzyme (ACE) inhibitors were found to be more effective in the treatment of LVH when compared to calcium channel blockers and beta blockers. ECHO was found to be the best method to diagnose LVH. In patients with stage I HTN, 47.1% had normal LVM. Around 53% of the subjects with stage I HTN and all with stage II HTN had abnormal LVM. Retinal changes were noted in 96.2% of abnormal LVM patients and 50% of normal LVM patients. A positive association between BMI and LVH (OR: 1.39) was also noted. BMI may positively influence LVH regression. The presence of retinopathy, in addition to LVH, suggests an increased chance of regression with anti-hypertensive treatment.

Determinants of Left Ventricular Hypertrophy in Hypertensive Patients: Identification of High-Risk Patients by Metabolic, Vascular, and Inflammatory Risk Factors

Left ventricular hypertrophy (LVH) is recognized as an independent predictor of cardiovascular morbidity and mortality in hypertensive patients. Thus, it is critical to understand the mechanisms underlying the development of LVH for formulation screening and treatment strategies. This study was designed to determine the association between echographically determined LVH measures and markers of inflammation, neurohormonal activity, glomerular function, oxidative stress, insulin resistance, and vascular endothelial function. In this study, 129 hypertensive subjects were evaluated for lipids, glucose, HbA1C, insulin, homeostasis model assessment-insulin resistance, C-reactive protein (CRP), urinary microalbumin, homocysteine, aldosterone, renin, and endothelin. LVH parameters including interventricular septum thickness, posterior wall thickness (PWT), and left ventricular mass index (LVMI) were assessed echographically. Serum aldosterone levels were significantly positively associated with left ventricular mass (LVM) and marginally positively associated with LVMI and PWT. Both LVM and LVMI were significantly elevated in subjects with high versus normal serum aldosterone levels (p = 0.018 for LVM and p = 0.050 for LVMI). Serum endothelin was positively associated with LVM and LVMI. In multiple linear regression analysis, aldosterone remained a significant predictor of LVM (standardized β = 0.229, p = 0.024), and endothelin a marginally significant predictor of LVM (standardized β = 0.178, p = 0.077). Among serum lipids, high-density lipoprotein cholesterol only had a significant inverse association with LVM and PWT. Homocysteine as well as CRP were significantly positively associated with LVM and LVMI in females. This study found that aldosterone and endothelin levels are the most important independent determinants of LVH in hypertensive subjects. These markers may be useful to identify asymptomatic hypertensive subjects at risk for heart failure.

Dietary Sodium Alters the Prevalence of Electrocardiogram Determined Left Ventricular Hypertrophy in Hypertension

Determination of left ventricular hypertrophy (LVH) via electrocardiogram (ECG) is a known independent risk factor for cardiovascular morbidity and mortality in hypertension (HTN). Dietary sodium and HTN are both associated with unfavorable alterations in left ventricular mass, however, to what extent their interplay affects ECG screening for LVH is unclear. The effects of controlled dietary sodium manipulation on ECG determinants of LVH in hypertensive subjects were evaluated using well-established voltage criteria for LVH. ECGs from 80 hypertensive subjects were evaluated following random sequence assignment to 7 days of high sodium (HS) intake (200 mEq/24 h), and then 7 days of low sodium (LS) intake (10 mEq/24 h). Sodium restriction over 7 days resulted in significant decreases in overall, and LVH-specific, ECG voltages. Most subjects exhibited decrements in overall ECG voltage with sodium restriction (72%); however, a smaller subset displayed higher voltages when on LS intake (28%). The prevalence of ECG-determined LVH was significantly lowered with LS diet (HS diet 22/80 (28%) vs. LS diet 8/80 (10%), P < 0.05). Subjects exhibiting reversal of LVH status with sodium restriction were younger, demonstrated salt sensitivity of blood pressure, and lower LVH-specific ECG voltage. Short-term dietary sodium fluctuations can significantly alter overall ECG voltage and the prevalence of ECG-determined LVH in hypertensive individuals. Inclusion of dietary sodium assessment when screening hypertensive subjects for LVH by ECG may improve the consistency of cardiac risk assessment.

Will the Lessons From Primary Aldosteronism Change the Treatment of Hypertension and Left Ventricular Hypertrophy?

The renin-angiotensin-aldosterone system effectively defends against volume depletion, but in most developed nations, dietary sodium is high, and aldosterone production should be suppressed. The syndrome of primary aldosteronism demonstrates the consequences of autonomous aldosterone production in a sodium-replete society. For many years, primary aldosteronism was thought to be an esoteric disorder only diagnosed by academicians at a handful of institutions worldwide. Conn, Biglieri, Bravo, and others characterized the syndrome and developed diagnostic strategies circa 1960–1980. Most clinicians, however, could not execute these algorithms, and management was unsatisfactory because of poor methods for localizing aldosterone production and limited options for medical management. Interest shifted to other mechanisms of hypertension, but during the last 20 years, the advent of commercial assays for renin and aldosterone, the broader use of adrenal vein sampling, and the development of selective aldosterone antagonists have rejuvenated interest in primary aldosteronism.1 Furthermore, end-organ damage is more severe in primary aldosteronism than in essential hypertension, and considerable evidence implicates the activation of mineralocorticoid receptors in these tissues as the mechanism. Implicit in this aldosterone renaissance is the importance of making the diagnosis of primary aldosteronism to allow implementation of tailored therapy. Proteinuria is more prevalent in patients with primary aldosteronism than in those with essential hypertension,2 and the excess proteinuria largely reverses after treatment with surgery or spironolactone.3 Thus, the benefits reaped from the detection of primary aldosteronism and the implementation of targeted therapy extend beyond optimal control of blood pressure. Another malady associated with primary aldosteronism is left ventricular (LV) hypertrophy (LVH).4 LVH is associated with adverse cardiovascular events and all-cause mortality.5 Therapy, which leads to regression of LVH in hypertensive subjects, reduces these risks.6 Despite the importance of LVH as a risk factor and the high prevalence of LVH in primary …

Indexation Criteria of Ventricular Mass and Predictive Role of Blood Pressure and Body Composition

There is no definite consensus on which indexation of left ventricular mass (LVM) should be used to better identify left ventricular hypertrophy (LVH). Left ventricular mass has been adjusted to height, to height2.7(h2.7) and to body surface area (BSA). The aims of the present study were to evaluate the prevalence of LVH according to different indexations and different cut-offs and to identify the most useful indexation of LVM to detect hypertension-related LVH. Echocardiographic LVH was defined as LVM to h2.7, LVM to BSA, LVM to height, LVM values in the upper 5th percentile of our gender-related LVM distribution, using different partition values suggested in previous population-based studies. Prevalence of LVH in the general population was 32% using the less restrictive criterion (LVH 49.2/46.7 g/m2.7), 15% with the criterion of LVH 116/104 g/m2, and 3.8% with the most restrictive one (LVH 134/110 g/m2). Prevalence of LVH in hypertensive subjects was almost twice than in normotensive subjects with all criteria. Only 20 subjects out of the 707 evaluated were found to have LVH with all six criteria. In multiple regression analysis SBP was independently associated with nonindexed LVM and was indexed to both BSA and h2.7. On the other hand, fat-free mass was a powerful predictor of nonindexed LVM or of LVM to BSA, whereas body mass index was the strongest predictor of LVM to h2.7. The indexation of LVM to BSA, possibly with the cut-off of LVH 116/104, is probably the best criterion for identifying blood pressure-related LVH.

Beta blockers and left ventricular hypertrophy in hypertension

It is now generally accepted that hypertension-induced left ventricular hypertrophy (LVH) represents a phenomenon of multifactorial origin. Antihypertensive therapy with beta-blocking drugs influences most of the factors involved in the control of left ventricular mass. Therefore, although initial animal experiments yielded conflicting results, it is not surprising that a great deal of evidence has been accumulated in clinical studies showing that succesful long-term antihypertensive treatment with beta blockers induces regression of LVH in hypertensive subjects. Differences in molecular structure among various beta-blocking agents do not seem to influence this property. On the contrary, the question of whether reversal of LVH represents a beneficial or harmful byproduct of antihypertensive treatment with beta blockers is still unanswered. Animal and clinical studies suggest that left ventricular systolic function is unchanged or even improved after regression of LVH, whereas the ability of the heart to withstand recurrence of hypertension is slightly reduced. Furthermore, development of LVH in hypertensive subjects is associated with abnormalities in diastolic function which are not reduced by reversal of LVH induced by antihypertensive treatment with beta blockers.