Hypertrophy In Hypertensive Heart Disease Research Articles

33. Association between QT Dispersion and Left Ventricular Hypertrophy in Hypertensive Heart Disease Patients

Background: The variation in QT length reflects regional repolarization differences in the heart. An Increased in QT dispersion is associated with an increased left ventricular mass index in hypertensive individuals. Objective: The aim of this study was to investigate association between QT dispersion and left ventricular hypertrophy (LVH) in hypertensive heart disease (HHD) individuals. Method: This study was a-single centre, retrospective study, included 47 patients with hypertension who had visited the cardiology clinic. Electrocardiography (EKG) and trans-thoracal echocardiography (TTE) were performed. Patients were divided into LVH group (27) and control group (20) based on TTE findings. Patients with valvular abnormalities, myocardial infarction, LV dysfunction, pericardial disease, arrhythmia related, and pulmonary disease were excluded from this study. Results: LVH was diagnosed in 31 (56%) of the patients by 2D echocardiography. The QT interval maximum was higher at 414.00 ± 59.87, than 396.19 ± 37.75 in the control group. Corrected QT (QTc) maximum in HHD group also higher at 448.08 ± 54.83 compared to control group in 421.67 ± 35.61. QT minimum and QTc minimum both are higher in HHD group at 350.40 ± 53.27 and 378.32 ± 43.00 respectively than in controlled group, at 339.05 ± 43.12 and 361.29 ± 45.26. There was no significant association in QT dispersion (p = 0.582) and QTc dispersion (p = 0.265) between HHD group and controlled group. Conclusion: The QT dispersion trend was narrowly higher in hypertensive patient with LVH in HHD group than the controlled group but it was statistically insignificant.

Phenotyping of hypertensive heart disease and hypertrophic cardiomyopathy using personalized 3D modelling and cardiac cine MRI.

Differential diagnosis of hypertensive heart disease (HHD) and hypertrophic cardiomyopathy (HCM) is clinically challenging but important for treatment management. This study aims to phenotype HHD and HCM in 3D+time domain by using a multiparametric motion-corrected personalized modeling algorithm and cardiac magnetic resonance (CMR). 44 CMR data, including 12 healthy, 16 HHD and 16 HCM cases, were examined. Multiple CMR phenotype data consisting of geometric and dynamic variables were extracted globally and regionally from the models over a full cardiac cycle for comparison against healthy models and clinical reports. Statistical classifications were used to identify the distinctive characteristics and disease subtypes with overlapping functional data, providing insights into the challenges for differential diagnosis of both types of disease. While HCM is characterized by localized extreme hypertrophy of the LV, wall thickening/contraction/strain was found to be normal and in sync, though it was occasionally exaggerated at normotrophic/less severely hypertrophic regions during systole to preserve the overall ejection fraction (EF) and systolic functionality. Additionally, we observed that hypertrophy in HHD could also be localized, although at less extreme conditions (i.e. more concentric). While fibrosis occurs mostly in those HCM cases with aortic obstruction, only minority of HHD patients were found affected by fibrosis. We demonstrate that subgroups of HHD (i.e. preserved and reduced EF: HHDpEF & HHDrEF) have different 3D+time CMR characteristics. While HHDpEF has cardiac functions in normal range, dilation and heart failure are indicated in HHDrEF as reflected by low LV wall thickening/contraction/strain and synchrony, as well as much reduced EF.

Hypertrophic cardiomyopathy and left ventricular hypertrophy in hypertensive heart disease with mildly reduced or preserved ejection fraction: insight from altered mechanics and native T1 mapping

To explore the relationship between extracellular volume (ECV), native T1, and systolic strain in hypertrophic cardiomyopathy (HCM) and hypertensive patients with left ventricular hypertrophy (HTN LVH) with mildly reduced or preserved ejection fraction. T1 mapping was performed in 45 patients with late gadolinium enhancement positive (LGE+) HCM (mean age, 53±6 years), 11 patients with LGE- (LGE-) HCM (mean age, 56±5 years), and 20 patients with HTN LVH (mean age, 55±6 years) on at 3 T magnetic resonance imaging (MRI) using the modified look-locker inversion-recovery (MOLLI) pulse sequence. Mean T1 value, ECV and circumferential strain parameters were determined for each patient. Overall, the HCM patients had higher native T1 values (1242.92±68.94) and ECV (0.31±0.05) in comparison to those of the HTN LVH patients (1197±46.80, 0.27±0.04; p<0.05). In the subgroup analysis, the HCM LGE+ patients had the highest native T1 values among the three groups. The HCM LGE+ patients had higher ECV than the LGE- patients. HCM LGE- patients had higher ECV than HTN LVH patients (p<0.05). Peak systolic circumferential strain and early diastolic strain rates were reduced in the HCM LGE+ patients in comparison to the HCM LGE- and HTN LVH patients (p<0.05). Reduced peak systolic and early diastolic circumferential strain rates were associated with increased levels of ECV and native T1 values among all the patients. HCM LGE+ patients had higher native T1 values, higher ECV, and an associated reduction in early diastolic strain rates and peak systolic circumferential strains when compared to the HCM LGE- and HTN LVH patients with mildly reduced or preserved ejection fraction.

0122 : Arrhythmic risk of hypertensive heart disease

Left ventricular hypertrophy in hypertensive heart disease favors the occurrence of atrial and ventricular arrhythmias that put the hemodynamic and embolic risk. The aim of our study was to investigate the prevalence of cardiac arrhythmias in this population and to offer sufficient support. This is a prospective, analytical 10 months including 144 hypertensive patients with and without LVH hypertensive. We placed these patients a HolterECG recording over 24 hours. We excluded all patients with other types of heart disease and those taking beta-blocker treatment and / or antiarrhythmic. The average age of our patients was 64 ± 8 years with female predominance. 66% of patients with LVH showed heart rhythm disorders versus 6% of patients without LVH. Ventricular premature beats occurred in 16.6% versus 4.3% with LVH without LVH, venabstricular tachycardia not supported in 2.7% with 0% LVH against the supraventricular extrasystoles occurred in 55.6% without LVH against 13.6%. ACFA and atrial tachycardia with LVH in 11.1% versus 1.1%. The variability of the heart rate was altered in 33% with LVH versus 6.6% without LVH. Arrhythmias represent the third face of hypertensive heart disease after coronary artery disease and heart failure. Holter ECG recording information on the three factors of atrial or ventricular arrhythmias: the trigger, the state of the autonomic nervous system and the search for silent ischemia. An early and effective management of hypertension is necessary to prevent the onset or regress left ventricular hypertrophy, determining factor in the genesis of these arrhythmias as atrial ventricular that.

Cardiac Magnetic Resonance Assessment of Interstitial Myocardial Fibrosis and Cardiomyocyte Hypertrophy in Hypertensive Mice Treated With Spironolactone

BackgroundNearly 50% of patients with heart failure (HF) have preserved LV ejection fraction, with interstitial fibrosis and cardiomyocyte hypertrophy as early manifestations of pressure overload. However, methods to assess both tissue characteristics dynamically and noninvasively with therapy are lacking. We measured the effects of mineralocorticoid receptor blockade on tissue phenotypes in LV pressure overload using cardiac magnetic resonance (CMR).Methods and ResultsMice were randomized to l‐nitro‐ω‐methyl ester (l‐NAME, 3 mg/mL in water; n=22), or l‐NAME with spironolactone (50 mg/kg/day in subcutaneous pellets; n=21). Myocardial extracellular volume (ECV; marker of diffuse interstitial fibrosis) and the intracellular lifetime of water (τic; marker of cardiomyocyte hypertrophy) were determined by CMR T1 imaging at baseline and after 7 weeks of therapy alongside histological assessments. Administration of l‐NAME induced hypertensive heart disease in mice, with increases in mean arterial pressure, LV mass, ECV, and τic compared with placebo‐treated controls, while LV ejection fraction was preserved (>50%). In comparison, animals receiving both spironolactone and l‐NAME (“l‐NAME+S”) showed less concentric remodeling, and a lower myocardial ECV and τic, indicating decreased interstitial fibrosis and cardiomyocyte hypertrophy (ECV: 0.43±0.09 for l‐NAME versus 0.25±0.03 for l‐NAME+S, P<0.001; τic: 0.42±0.11 for l‐NAME groups versus 0.12±0.05 for l‐NAME+S group). Mice treated with a combination of l‐NAME and spironolactone were similar to placebo‐treated controls at 7 weeks.ConclusionsSpironolactone attenuates interstitial fibrosis and cardiomyocyte hypertrophy in hypertensive heart disease. CMR can phenotype myocardial tissue remodeling in pressure‐overload, furthering our understanding of HF progression.

Elevated extracellular volume and arterial stiffness are associated with left ventricular hypertrophy in hypertensive heart disease

Background: To determine interconnection between serum none heme iron levels and different functional classes of chronic heart failure (CHF) in hypertensives with anemia. Methods: This study included 79 hypertensives (28 male, 51 female; age 53.11 7.97 years) with CHF Class II-III NYHA with preserved left ventricular ejection fraction (LVEF >50%). All patients were divided into 2 groups accordingly to the presence symptoms and signs of anemia: 24 patients without anemia (group I) and 55 patients with anemia (group II). There were patients with CHF Class II (NYHA) (subgroup A) and CHF Class III (subgroup B) in each group. Complete blood count [haemoglobin (Hb), erythrocytes (Er)], serum iron, ferritin and transferrin levels by ELISA methods were measured. Control group consisted of 20 healthy people. Results: Patients in group I have normal blood Hb and Er levels in the range of 123.71 7.42 g/L and 4.27 0.69 1012/L vs. 120.35 2.05 g/L and 3.79 0.93 1012/L in the control group (p>0.05). Patients in group II have Hb and Er levels lower by 26.19% and 28.98% accordingly vs. the control group (p0.05). In group IB serum iron, ferritin and transferrin levels were lower by 19.95%; 22.32% and 10.12% accordingly vs. the patients in group IA (p<0.05). In group IIA serum iron, ferritin and transferrin levels were equal to 10.56 3.88 mmol/L; 61.14 8.26 mcU/L and 2.18 0.18 g/L accordingly and were lover vs. group IA and IB (p<0.05). In group IIB serum iron, ferritin and transferrin levels were lower by 25.37%; 12.87% and 16.05% accordingly vs. the patients in group IIA (p<0.05). Conclusions: The serum non heme iron levels depend on the functional class of CHF. There is a necessity to identify the iron deficiency states by measuring not only the indexes of serum iron, but also ferritin and transferrin levels. Serum concentration of none heme iron is useful marker in the diagnostic and treatment effectiveness of anemia in hypertensives with CHF.

Increased extracellular volume and altered mechanics are associated with left ventricular hypertrophy in hypertensive heart disease, not hypertension alone

Background Study purpose To detect differences in extracellular volume (ECV) and systolic strain in hypertensive patients with LVH as compared to hypertensive patients without LVH and age-matched controls. Background: Increased ECV due to diffuse myocardial fibrosis in hypertensive patients may be an underlying mechanism contributing to increased cardiovascular risk. Moreover HTN patients with left ventricular hypertrophy (LVH) are at higher risk of cardiovascular morbidity and mortality when compared to HTN Non-LVH subjects. We compared levels of ECV and systolic strain between HTN LVH, HTN Non-LVH and control subjects.

Inactivation of the immune receptor CD40 attenuates the development of cardiac hypertrophy in angiotensin-II induced hypertensive heart disease

Emerging evidence indicates that inflammatory activation is a crucial pathway in disease progression during HF. The co-stimulatory dyad CD40-CD40L is involved in pro-inflammatory activation of a wide range of immune and non-immune cells and plasma levels of soluble CD40L in HF patients are raised. Here we investigated whether CD40-CD40L interactions attenuate cardiac hypertrophy in hypertensive heart disease. CD40 knockout and wild type C57Bl6-J mice were treated with angiotensin II (AngII, 2.5 mg/kg/day) for 4 weeks. AngII-induced hypertension led to a significant increase in cardiac mass in Wt mice (+31%, P<0.01), but not in CD40 knockout mice (+10%, N.S.). Comparable changes were observed in diastolic wall thickness (echocardiography) and cardiomyocyte cross sectional area. To determine which CD40-TRAF interactions were involved, the effect of mutations in the intracellular TRAF binding domains of CD40 was investigated. Relative to mice with intact downstream CD40 signaling, disruption of TRAF2/3/5, TRAF6 or both binding sites was associated with reduced cardiac hypertrophy (cardiac mass -24% for CD40-TΔ2, -28% for CD40-TΔ6 and -26% in CD40-TΔ2/6; p<0.05). Reduced hypertrophy was not associated with a decline in immune cell infiltration (CD45+ cells) or collagen content. Although the exact mechanism remains to be elucidated the present findings indicate a role for the CD40 receptor in the development of cardiac hypertrophy.

CD40‐CD40 ligand (CD40L) signaling modulates cardiac hypertrophy in angiotensin‐II induced hypertensive heart disease

The co‐stimulatory dyad CD40‐CD40L is involved in pro‐inflammatory activation of a wide range of immune and non‐immune cells. Here we investigated whether CD40‐CD40L interactions attenuate cardiac hypertrophy in hypertensive heart disease. Therefore CD40 knockout and wild type C57Bl6‐J mice were treated with angiotensin II (AngII) (2.5 mg/kg/day) for 4 weeks. AngII‐induced hypertension led to a significant increase in cardiac mass in Wt mice (+31%, P&lt;0.01), but not in CD40 knockout mice (+10%, N.S.). Comparable changes were observed in diastolic wall thickness (echocardiography) and cardiomyocyte cross sectional area. To determine which CD40‐TRAF interactions were involved, the effect of mutations in the intracellular TRAF binding domains of CD40 was investigated. Relative to mice with intact downstream CD40 signaling, disruption of TRAF2/3/5, TRAF6 or both binding sites was associated with reduced hypertrophy (cardiac mass −24% for CD40‐TΔ2, −28% for CD40‐ TΔ6 and −26% in CD40‐TΔ2/6; p&lt;0.05). Reduced hypertrophy was not associated with a decline in immune cell infiltration (CD45+ cells) or collagen content. Although the exact mechanism remains to be elucidated the present findings indicate that CD40‐ CD40L interactions are involved in the development of cardiac hypertrophy.

Mechanisms of Disease: pathologic structural remodeling is more than adaptive hypertrophy in hypertensive heart disease

Changes in the composition of cardiac tissue develop in arterial hypertension and lead to structural remodeling of the myocardium. Structural remodeling is the consequence of a number of pathologic processes, mediated by mechanical, neurohormonal and cytokine routes, occurring in the cardiomyocyte and the noncardiomyocyte compartments of the heart. One of these processes is related to the disruption of the equilibrium between the synthesis and degradation of collagen type I and III molecules, which results in an excessive accumulation of collagen type I and III fibers in the interstitium and the perivascular regions of the myocardium. The clinical relevance of ventricular fibrosis is that it might contribute to the increased cardiac risk of patients with hypertensive heart disease. This review focuses on the mechanisms of hypertensive ventricular fibrosis and its clinical consequences. In addition, we discuss the noninvasive methods for the diagnosis of cardiac fibrosis and the therapeutic strategies aimed to promote its reduction.

Regression of Myocardial and Coronary Vascular Hypertrophy in Hypertensive Heart Disease

In essential hypertension, ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by the organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Coronary reserve is reduced even in hypertensive hypertrophy without evidence of coronary artery disease. MVO2 per mass unit is directly correlated with systolic wall stress per cross-sectional area of the left ventricular wall. It is concluded that the appropriateness of left ventricular hypertrophy, as a result of mass-to-volume ratio and stress, is a major determinant of left ventricular performance, of coronary blood flow, and of myocardial oxygen consumption. Pharmacotherapeutical means of reversing cardiac hypertrophy (prazosin, clonidine, enalapril, and nifedipine) were analyzed in concentrically, as well as eccentrically, hypertrophied left ventricles. Regression of cardiac hypertrophy, i.e., therapeutic intervention on a critical precursor of hypertensive congestive heart failure, can be obtained by various antihypertensive agents. Prazosin, calcium channel blockers, and angiotensin converting enzyme inhibitors as well as a combined treatment regimen using alpha-receptor blockers together with diuretics and vasodilators can all induce regression of hypertrophy associated with an improvement in left ventricular function. Moreover, an improved coronary reserve may reduce the ischemic risk of the hypertrophied myocardium. However, not all antihypertensive drugs seem equally effective in bringing about coronary regression of left ventricular hypertrophy (LVH). No regression or little regression has been found with diuretic monotherapy despite a satisfactory reduction in blood pressure. On the other hand, a trend towards a regression has been observed in patients in whom treatment with clonidine significantly reduced catecholamines. Recent experimental data in spontaneously hypertensive rats indicate that the impaired coronary reserve can be significantly improved by the long-term administration of blood pressure lowering agents, e.g., by nifedipine or by the combination of metoprolol plus hydralazine.

A Comparison of Echocardiography and Electrocardiography in the Diagnosis of Left Ventricular Hypertrophy in Hypertensive Heart Disease

A Comparison of Echocardiography and Electrocardiography in the Diagnosis of Left Ventricular Hypertrophy in Hypertensive Heart Disease

Sequential changes in the development of the electrocardiographic pattern of left ventricular hypertrophy in hypertensive heart disease

A lthough recent reviews1-5 have summarized the available data concerning the diagnostic value of the electrocardiogram in left ventricular hypertrophy, little attention has been directed toward the sequential changes in the development of this pattern. Much of the controversy concerning the significance of the electrocardiographic pattern of left ventricular hypertrophy has centered upon the interpretation of ST-T changes. The problem of long standing6-* is whether the ST-T abnormalities are purely secondary to the increasing magnitude of the QRS vector or whether they represent an additional complication. Adequate analysis of these relationships would be enhanced by clinical electrocardiographic correlations over the entire lifespan of developing hypertrophy. Long-range electrocardiographic studies have been hampered since routine precordial leads have only been available since 1945. The present material consists of such studies of developing hy-pertrophy in 22 patients.