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PubMed1993

Erythrocyte ion fluxes in essential hypertensive patients with left ventricular hypertrophy.

BACKGROUND: Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular morbidity and mortality in essential hypertension (EH). Several hemodynamic and nonhemodynamic factors have been involved in the development of LVH in hypertension, including abnormalities in cellular ion mobilization. METHODS AND RESULTS: We measured different ion transport systems in erythrocytes from 50 patients with EH classified as having or not having LVH measured by M-mode echocardiography. Thirty-two EH patients (64%) exhibited criteria of LVH, and 18 (36%) did not. When the two groups were compared, patients with LVH were older (44.7 +/- 7.4 versus 37.6 +/- 9.2 years; P < .01) and exhibited higher rates of erythrocyte Na(+)-H+ exchange (9.8 +/- 4.1 versus 7.1 +/- 2.6 mmol.[L.cells.h]-1; P < .05) and higher intraerythrocyte Na+ content (8.5 +/- 1.3 versus 7.5 +/- 0.8 mmol/L per cell; P < .01). Systolic and diastolic blood pressure values, as well as biochemical, hormonal, and other erythrocyte ion transport systems studied did not differ between EH with or without LVH. The results of a multiple linear regression analysis using left ventricular mass index (LVMI) as the dependent variable showed that Na(+)-H+ exchange and the maximal rate of the Na(+)-K(+)-Cl- cotransport were the only two independently significant parameters associated with an increased LVMI. CONCLUSIONS: The increased rate of the erythrocyte Na(+)-H+ exchange and the decreased maximal rate of the Na(+)-K(+)-Cl- cotransport system are both associated with the presence of LVH in EH patients. These abnormalities of ion transport pathways tend to increase the intracellular Na+ content and may be involved in the pathogenesis of LVH in EH.

Adult↗
PubMed1983

Abnormal diastolic left ventricular posterior wall motion in left ventricular hypertrophy.

The left ventricular pressure-volume relationship is abnormal in left ventricular hypertrophy (LVH). As a result, the left atrium empties more slowly than normal during the rapid filling phase of diastole, producing a characteristic abnormality of diastolic aortic root motion. In order to determine whether this altered LV filling is accompanied by a derangement of diastolic LV wall motion which might be useful in identifying the presence of altered chamber compliance, the M-mode echocardiograms of 60 patients with LVH secondary to aortic stenosis, hypertrophic subaortic stenosis, or hypertension, and those of 36 normal individuals were evaluated. Patients with LVH demonstrated abnormal LV posterior wall motion manifested by prolonged phases of rapid ventricular filling and atrial contraction (p less than 0.01 and p less than 0.05, respectively). The early diastolic wall motion abnormality can be readily detected by visual inspection of the echocardiogram. These findings support the concept of diastolic dysfunction in LVH and represent another echocardiographic feature of that condition.

Adult↗
PubMed1990

Clinical studies of drug reversal of hypertensive left ventricular hypertrophy.

Because left ventricular hypertrophy (LVH) is a strong risk factor for cardiac morbidity and mortality considerable interest has been generated concerning the possible effects of modifying LVH in hypertensive patients. In animal models disproportionate regression of left ventricular (LV) mass in relation to blood pressure may produce adverse effects on coronary blood flow reserve or LV systolic function. Clinical studies of modulation of LVH with antihypertensive drug therapy have been of two types: (1) large scale community comparison trials in which the prevalence of LVH and its regression were evaluated serially by electrocardiography (ECG) with stepped care drug therapy and (2) relatively short term (less than 2 years) studies with echocardiographic (ECHO) determination of LVH. The development of anatomically validated measurement of LV muscle mass by ECHO has demonstrated ECHO to be much more sensitive than ECG to assessment of LVH. Community comparison trials of stepped care therapy such as the Multiple Risk Factor Intervention Trial (MRFIT) and Hypertension Detection and Followup Study (HDFP) have not had the statistical power to demonstrate significant effects on risk reduction despite evidence for significant decrease in ECG-LVH despite participant numbers in the range of 8,000 to 10,000 followed serially for 5 to 6 years. Analysis of over 60 studies of hypertensive treatment using ECHO for assessment of LVH mass changes, averaging 10 to 15 subjects/study, indicates that correlation of reduction of LV mass with decrease in blood pressure has been weak (r = 0.255, P less than .025). Drug monotherapy studies have shown that use of calcium channel blockers and angiotensin converting enzyme inhibitors predominantly decrease LV mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive Agents↗
PubMed2002

Comparison of actions of irbesartan versus atenolol on cardiac repolarization in hypertensive left ventricular hypertrophy: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation Versus Atenolol (SILVHIA).

Left ventricular (LV) hypertrophy is associated with a substantial risk for malignant arrhythmias and sudden death. The effects of antihypertensive therapy on QT dispersion, which reflects cardiac repolarization heterogeneity, in relation to changes in LV mass has not been well studied. Repeat echocardiography and QT measurements (standard 12-lead electrocardiograms) were performed in hypertensive patients with LV hypertrophy, who were randomized double-blind to receive the angiotensin II type 1-receptor blocker irbesartan (n = 44) or the beta(1)-receptor blocker atenolol (n = 48) for 48 weeks, and in 37 matched hypertensive control subjects without LV hypertrophy. LV mass index was related to QT dispersion (r = 0.34, p <0.001). The reduction in LV mass was greater using irbesartan than using atenolol (-27 +/- 28 vs -15 +/- 21 g/m(2) at 48 weeks, p = 0.021), with similar reductions in blood pressure. Irbesartan decreased QT dispersion (from 56 +/- 24 ms to 45 +/- 20 ms at 48 weeks; p <0.001) and QTc dispersion (from 57 +/- 24 to 44 +/- 19 ms at 48 weeks; p <0.001). In contrast, atenolol had minor effects. The decreases in QT and QTc dispersions were greater using irbesartan than using atenolol (p = 0.001 and p = 0.011, respectively); the same results were found when changes in LV mass, blood pressure, and heart rate were also included in multivariate analyses. Thus, heterogeneity of ventricular repolarization is related to the degree of LV hypertrophy. Irbesartan, but not atenolol, reduces QT and QTc dispersions independent of changes in LV mass, blood pressure, or heart rate, and thus seems to induce structural and electrical remodeling in a direction that could decrease the risk of fatal events in hypertensive patients.

Adrenergic beta-Antagonists↗
PubMed1984

Left ventricular hypertrophy in left bundle branch block.

The detection of left ventricular hypertrophy (LVH) in the presence of left bundle branch block (LBBB) remains a difficult clinical problem. Its prevalence and significance have not previously been studied in a group of living patients. M-mode echocardiography was utilized to determine the prevalence of anatomic LVH in 28 patients with LBBB. Various ECG and chest x-ray criteria as predictors of LVH were assessed. Anatomic LVH was present in 89% by echocardiography. A left atrial abnormality on ECG and a cardio-thoracic ratio greater than .50 were the best predictors of LVH. Hypertension and/or ischemic heart disease was present in 78.5% of the patients while only one patient was free of any evidence of cardiovascular disease.

Aged↗
PubMed2003

Relation between cardiac sympathetic activity and hypertensive left ventricular hypertrophy.

BACKGROUND: Left ventricular (LV) hypertrophy is an independent risk factor for cardiovascular morbidity and mortality in hypertensive subjects. Sympathetic activation has been suggested to contribute to LV hypertrophy, but this has not yet been conclusively validated in humans. METHODS AND RESULTS: We comprehensively assessed total systemic and regional sympathetic activity by radiotracer dilution methods and microneurography in 15 untreated hypertensive subjects with echocardiographic evidence of LV hypertrophy (EH+), 11 hypertensive subjects with similar blood pressure but without LV hypertrophy (EH-), and 10 age-matched normotensive control subjects (NT). LV mass index was 87+/-15 g/m2 in NT, 106+/-11 g/m2 in EH-, and 138+/-17 g/m2 in EH+ (P<0.001). Total body and renal norepinephrine spillover were higher in both hypertensive groups compared with NT (total norepinephrine spillover, NT 223+/-145 versus EH- 418+/-135 versus EH+ 497+/-303 ng/min; renal norepinephrine spillover, NT 38.8+/-25.3 versus EH- 88.6+/-58.0 versus EH+ 103.4+/-56.2 ng/min; both P<0.05). However, muscle sympathetic nerve activity (NT 25+/-6 versus EH- 38+/-20 versus EH+ 57+/-19 bursts per 100 heartbeats; P<0.01) and cardiac norepinephrine spillover (NT 11.7+/-6.2 versus EH- 13.1+/-7.2 versus EH+ 28.6+/-17.4 ng/min; P<0.01) were only increased in EH+. Cardiac norepinephrine spillover correlated positively with LV mass index in all subjects (r=0.52; P<0.001). CONCLUSIONS: Our findings demonstrate that hypertensive LV hypertrophy is associated with increased sympathetic activity largely confined to the heart, suggesting that increased cardiac norepinephrine release is related to the development of LV hypertrophy.

Adult↗
PubMed2006

Tissue velocity echocardiography shows early improvement in diastolic function with irbesartan and atenolol therapy in patients with hypertensive left ventricular hypertrophy. Results form the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA).

BACKGROUND: Abnormal diastolic function is common in hypertensive left ventricular hypertrophy (LVH). Early identification and treatment may prevent future cardiovascular events. METHODS: We examined 58 hypertensive patients with LVH, 38 with hypertension but no LVH, and 38 normotensive subjects. The effects of the AT1 receptor blocker irbesartan and the beta1 blocker atenolol on diastolic function during 48 weeks of treatment were evaluated in the LVH group by tissue velocity echocardiography (TVE). We measured basal septal and lateral wall velocities of early (Em) and late (Am) diastolic myocardial wall motion, Em velocity deceleration time (E-decm), and isovolumic relaxation time (IVRTm). For comparison, diastolic function was assessed by conventional mitral pulse wave Doppler echocardiography. RESULTS: Diastolic function was impaired in both hypertensive groups. Irbesartan and atenolol (week 48, septal wall) improved IVRTm (-44%, P<.001, and -19%, P<.001; P<or=.001 between groups), E-decm (+56%, P<.001, and +53%, P<.001), and Em/Am (+11%, P=.396, and +20%, P=.010). Only irbesartan improved E/Em (-4%, P=.052 v +2%, P=.041). For irbesartan, relative changes in IVRTm and in septum thickness were related (P=.017), whereas relative changes in the Em/Am ratio and in heart rate were related for atenolol (P=.027). Alterations in diastolic dysfunction were greater and detected earlier with TVE than with conventional echocardiography. CONCLUSIONS: The TVE is more sensitive than conventional echocardiography in detecting alterations in diastolic function. Both irbesartan and atenolol improve diastolic function, but through different mechanisms. The improvement in IVRTm was greater with irbesartan, and only irbesartan improved E/Em. This may have implications on the treatment of high risk hypertensive patients.

Adrenergic beta-Antagonists↗
PubMed2003

[Left ventricular hypertrophy in hypertension. Part II. Prognostic value of left ventricular hypertrophy].

This part of review is based on results of prospective studies of prognostic value of left ventricular hypertrophy defined by electro- or echocardiographical criteria. Increased risk of cardiovascular complications has been found to be associated with left ventricular hypertrophy detected not only by voltage ECG criteria but also by ST-segment and T-wave changes in left precordial leads. Left ventricular myocardial mass is an independent factor of prognosis too. Prognostic significance of left ventricular hypertrophy depends on echocardiographical criteria used and on age, sex, race of patients and presence of coronary heart disease. Unfavorable prognostic significance of left ventricular hypertrophy becomes evident after several years of follow-up. Concentric left ventricular remodeling is also associated with increased risk of cardiovascular complications, however its value for prognosis is inferior to that of left ventricular hypertrophy.

Echocardiography↗
PubMed1993

[Ventricular arrhythmia and sudden cardiac death: the significance of left ventricular hypertrophy as risk factor].

Left ventricular hypertrophy is a frequent and early manifestation of cardiac structural adaptation in patients with essential hypertension. Prospective studies have clearly demonstrated that left ventricular hypertrophy represents a risk factor for cardiovascular morbidity and mortality, including sudden cardiac death. The increased risk is independent of the impact of high blood pressure and other risk factors on the cardiovascular system. Various clinical studies noted increased prevalence and severity of premature ventricular beats in hypertensive patients with left ventricular hypertrophy. Hypertrophy of myocardial cells, dilation of the left ventricle, increased stress of subendocardial myocardium and impaired coronary reserve are discussed as a possible pathogenetic link between myocardial hypertrophy and ventricular arrhythmias. Therapeutically, the primary goal for ventricular arrhythmias in hypertensive patients with left ventricular hypertrophy is regression of left ventricular mass. For this purpose, centrally sympatholytic agents, angiotensin converting enzyme inhibitors, betablockers and calcium antagonists have been found to be effective. Recently we observed that a reduction of left ventricular hypertrophy was associated with a decreased prevalence and severity of ventricular arrhythmias. Nevertheless, prospective studies are required to demonstrate whether reduction of severe ventricular arrhythmias helps to prevent sudden cardiac death due to left ventricular hypertrophy in hypertension.

Antihypertensive Agents↗
PubMed2004

[Left Ventricular Hypertrophy in Hypertension. Part III. Reversibility of Left Ventricular Hypertrophy During Treatment With Antihypertensive Drugs].

Results of prospective trials of effects of various antihypertensive drugs on left ventricular hypertrophy in patients with hypertensive disease are reviewed. According to 2 meta-analyses angiotensin converting enzyme inhibitors are most effective inducers of regression of left ventricular hypertrophy. However in comparative randomized trials in patients with hypertension ability of diuretics, lipophilic beta-adrenoblockers, long-acting calcium antagonists, and angiotensin receptor blockers to cause regression of left ventricular hypertrophy was not inferior to that of angiotensin converting enzyme inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Heterogeneous signal intensity in magnetic resonance images of hypertrophied left ventricular myocardium.

Left ventricular hypertrophy is associated with decreased longevity and often leads to congestive heart failure. An exploratory study of magnetic resonance imaging in human left ventricular hypertrophy was performed. First, 13 patients with left ventricular hypertrophy and 7 controls of similar ages were studied using electrocardiogramgated end-diastolic images. Visual inspection suggested that low-intensity zones were frequently found within the hypertrophied myocardium. To verify this observation, the images were processed with semi-automatic edge detection and a derivative-based tissue characterization algorithm, yielding tissue heterogeneity indices (THI-A and THI-V) which objectively measured the low-intensity zones. THI-A and THI-V were both significantly greater in left ventricular hypertrophy patients than in controls (THI-A: 0.111 vs 0.038, p = 0.009). THI was also significantly correlated with duration of disease and electrocardiographic abnormalities. To validate these initial findings prospectively, the same quantitative analysis was applied to magnetic resonance images of an additional 20 left ventricular hypertrophy patients and 12 controls from two institutions, using different imaging systems and different acquisition parameters. Again, THI was significantly greater in patients than in controls. Analysis of end-systolic images yielded similar results. In four dogs with left ventricular hypertrophy induced by aortic banding, THI showed a statistically significant increase as left ventricular hypertrophy developed. Hypertrophied myocardium thus shows reproducible differences from normal tissue with magnetic resonance imaging; hence, quantitative magnetic resonance tissue characterization may be useful in assessing pathologic changes in LVH.

Adult↗
PubMed2005

[Assessment of coronary reserve in patients with hypertensive disease and without hypertrophy left ventricular].

AIM: To study relationship between coronary reserve and left ventricular geometry. METHOD AND MATERIAL: Transesophageal cardiac pacing was carried out in 53 patients with hypertensive disease. Thirty five patients (66%) had left ventricular hypertrophy which was eccentric in 16 and concentric in 19. RESULTS: Myocardial ischemia was induced during pacing in 79.2% of patients; it was painful in 45.2 and painless -- in 54.8% of patients. Test with esophageal pacing was positive in 91.4 and 55.6% of patients with and without left ventricular hypertrophy, respectively. In patients with concentric hypertrophy frequency of positive tests was higher and level of coronary reserve lower than in patients with eccentric left ventricular hypertrophy. There was negative correlation between pacing rate at myocardial ischemia induction and left ventricular myocardial mass index. Painless ischemia was more frequent among patients with left ventricular hypertrophy. Twelve of 42 patients (28.3%) with positive result of pacing had no clinical signs of ischemic heart disease. CONCLUSION: Left ventricular hypertrophy limits coronary reserve, increases prevalence of painless myocardial ischemia. Transesophageal pacing enables detection of preclinical signs of lowered coronary reserve.

Adult↗
PubMed1995

Heart rate variability in left ventricular hypertrophy.

BACKGROUND: Electrocardiographic left ventricular hypertrophy and strain are associated with increased cardiac morbidity and mortality. Impaired cardiac autonomic function, assessed non-invasively by spontaneous heart rate variability on Holter monitoring, is associated with an increased risk of sudden death after myocardial infarction. AIM: To study the effect of left ventricular hypertrophy on heart rate variability. PATIENTS: 36 controls and 154 patients with left ventricular hypertrophy (94 with hypertension and 60 with aortic valve disease). SETTING: Tertiary referral centre. METHODS: Heart rate variability was measured on 24 h Holter recordings by non-spectral methods. Left ventricular mass index and fractional shortening were measured by echocardiography. RESULTS: Patients with left ventricular hypertrophy had a higher left ventricular mass index (P < 0.001) and reduced heart rate variability (P < 0.001) compared with those of the controls. A continuous inverse relation was apparent between heart rate variability and left ventricular mass index (r = -0.478, P < 0.001). Heart rate variability was not affected by age, the presence of coronary artery disease in patients with left ventricular hypertrophy, or beta blocker treatment for hypertension. Multivariate analysis showed that left ventricular mass index is the most important determinant of heart rate variability. CONCLUSION: Heart rate variability is significantly reduced in patients with left ventricular hypertrophy secondary to hypertension or aortic valve disease. A continuous inverse relation exists between heart rate variability and left ventricular mass index. Impaired cardiac autonomic function in left ventricular hypertrophy may contribute to the mechanism of sudden death.

Aortic Valve Stenosis↗
PubMed1998

Pathological versus physiological left ventricular hypertrophy: a review.

Left ventricular hypertrophy is recognized as an independent risk factor for cardiovascular morbid events. The primary mechanisms responsible for stimulating it are unknown. Epidemiological theories suggest that left ventricular hypertrophy is a continuous variable with no threshold, while morphological studies argue that it is the structure, or quality, and function of the myocardium (and therefore non-continuous), not the quantity of the myocardial mass, that poses the cardiovascular risk. Although left ventricular hypertrophy has been classically viewed as an adaptive response of the cardiovascular system to an imposed load, it has been demonstrated that haemodynamic overloading in selected hypertensive patients is not the sole determinant of left ventricular structure and function. Pathological and physiological states of left ventricular hypertrophy have been described primarily using criteria focusing on normal chamber performance and oxygen delivery as well as the reversibility of the hypertrophy once the overload is removed. Both states are also defined by the nature of the imposed load and the resulting myocardial adaptations. This review addresses the pathological and physiological states of left ventricular hypertrophy, the hypertrophy patterns, and the corresponding structural and functional characteristics, together with some of the biochemical factors thought to influence remodelling.

Cardiomyopathy, Hypertrophic↗
PubMed1991

Angiotensin-converting enzyme inhibition, cell growth, and left ventricular hypertrophy in hypertension.

Left ventricular hypertrophy is now recognized as an important risk marker in cardiovascular morbidity and mortality. Left ventricular hypertrophy is an integral component of the complex pathophysiology of primary hypertension and results from mechanical, neurohumoral, and genetic factors. The renin-angiotensin system is involved with the production of left ventricular hypertrophy, not only through the effects on systemic arterial blood pressure but also by both direct and indirect effects on myocardial cell growth. The angiotensin-converting enzyme (ACE) inhibitors are effective drugs for reducing blood pressure in primary hypertension. ACE inhibitor therapy is also associated with regression of left ventricular hypertrophy and restoration of normal diastolic and systolic left ventricular function. Regression of left ventricular hypertrophy is associated with improved prognosis. Thus, when left ventricular hypertrophy regression is a goal of antihypertensive treatment, the ACE inhibitors are effective drugs.

Angiotensin-Converting Enzyme Inhibitors↗