Ventricular Hypertrophy In Hypertensive Patients Research Articles

Common Carotid Artery Stiffness and Patterns of Left Ventricular Hypertrophy in Hypertensive Patients

The aim of this study was to determine the relationship between the lumen diameter and function of the common carotid artery, a vessel representative of the capacitance portion of the circulation, and the different patterns of left ventricular hypertrophy in uncomplicated essential hypertensive patients. Carotid luminal diastolic cross-sectional area, distensibility, and compliance were derived from measurements by a high-definition echotracking system. Left ventricular dimensions were from echocardiography. The 86 hypertensive patients included 31 who had never been treated (group 1), 31 in whom treatment had been stopped for at least 2 weeks (group 2), and 24 treated patients (group 3). In multivariate analysis of the population as a whole, the following relations were statistically independent of age, blood pressure, gender, and group: Left ventricular end-diastolic volume index was positively correlated to carotid luminal cross-sectional area (r = .46, P < .0001) and compliance (r = .47, P < .0001); left ventricular mean wall thickness and mass-volume ratio were negatively correlated to distensibility (r = -.68, P < .0001; r = -.46, P < .0001, respectively) and compliance (r = -.40, P < .0001; r = -.37; P < .001, respectively); and left ventricular mass index was positively correlated to luminal cross-sectional area (r = .23, P < .02) and negatively to distensibility (r = -.26, P < .01). These results indicate that geometric and functional changes in the common carotid artery accompany geometric changes in the left ventricle. More specifically, they suggest that a reduction in distensibility paralleled cardiac concentric hypertrophy and remodeling, whereas an increase in arterial volume paralleled increased left ventricular cavity size.

Effects of one-year treatment with rilmenidine on systemic hypertension-induced left ventricular hypertrophy in hypertensive patients

In patients with essential hypertension, left ventricular hypertrophy (LVH) increases the risk for cardiovascular morbidity and mortality. Thus its reversal represents one of the principal endpoints of antihypertensive treatment. We assessed the cardiovascular effects of 1-year antihypertensive treatment with rilmenidine (1 or 2 mg/day orally), a new oxazoline with a potent antihypertensive action that acts selectively through imidazoline-preferring receptors. In 11 hypertensive patients (mean age, 49 ± 2 years) with LVH, we measured systemic hemodynamics, large artery compliance, cardiac anatomy, and endocrine function. Patients underwent M-mode and 2-dimensional echocardiography as well as Doppler and peripheral pulsed Doppler flowmetry, determination of plasma atrial natriuretic factor (ANF) levels and renin activity (PRA), and of 24-hour urinary electrolyte and creatinine excretion in control conditions (systolic/diastolic blood pressure, 148 ± 3 102 ± 1 mm Hg ), 4 weeks after blood pressure normalization ( 131 ± 2 84 ± 2 mm Hg ; p < 0.01), after 1 year of satisfactory antihypertensive treatment ( 142 ± 3 90 ± 1 mm Hg ; p <0.01) and, finally, 1 month after therapy withdrawal ( 155 ± 3 106 ± 2 mm Hg ; difference not significant [NS]). One-year of rilmenidine treatment induced an improvement in brachial artery compliance (from 0.92 ± 0.06 to 1.16 ± 0.08 cm 4/dyne; p <0.05), which persisted after withdrawal of treatment (1.17 ± 0.06 cm 4/ dyne; p <0.05). LVH was reversed after 1 year of rilmenidine treatment (from 152 ± 5 to 131 ± 4 g/m 2 body surface area; p <0.05). Finally, PRA and urinary electrolyte excretion did not change throughout the study, and ANF remained unchanged after blood pressure normalization (48.4 ± 6.2 vs 44.7 ± 2.9 pg/mL; difference not significant) but fell after reversal of LVH (28.6 ± 3.4 pg/mL; p <0.05) and remained significantly lower than in control conditions after therapy withdrawal (27.5 ± 2.9 pg/mL; p <0.05). Our results demonstrate that long-term antihypertensive treatment with rilmenidine is able to induce a reversal of LVH and of the vascular structural changes associated with essential hypertension. In addition, they indicate that rilmenidine-induced regression of LVH is associated with significant and persistent reduction of ANF levels, which may suggest a favorable influence of the drug with the biosynthetic properties of ventricular myocardium.

Insulin-like growth factor-1 and cardiac mass in essential hypertension

Preliminary studies have shown that patients with essential hypertension and left ventricular hypertrophy have an excess of circulating insulin-like growth factor-1 (IGF-1). In addition, an association has been found between the decrease in IGF-1 after antihypertensive treatment and regression of left ventricular hypertrophy. To determine whether the effect of angiotensin converting enzyme (ACE) inhibitors on left ventricular hypertrophy in patients with essential hypertension is related to ACE inhibitor effects on IGF-1 levels. The relationship between echocardiographically determined left ventricular hypertrophy and plasma IGF-1 levels was investigated in 87 patients with essential hypertension before and after 6 months of randomly allocated treatment with captopril (n = 30), lisinopril (n = 37) or quinapril (n = 20). The control group consisted of 30 age- and sex-matched normotensive subjects without left ventricular hypertrophy. Baseline IGF-1 levels were higher in hypertensive patients than in normotensive controls (280 +/- 21 versus 240 +/- 15 ng/ml, means +/- SEM, P < 0.02). IGF-1 levels were higher in hypertensive patients with left ventricular hypertrophy (n = 25, 316 +/- 41 ng/ml) than in those without left ventricular hypertrophy (n = 62, 242 +/- 16 ng/ml, P < 0.05). There was a direct correlation between baseline IGF-1 and left ventricular mass in the hypertensive patients (r = 0.365, P < 0.001). All three ACE inhibitors caused similar reductions in IGF-1 levels, the left ventricular mass index and blood pressure after the treatment period. The effect of ACE inhibition on mean blood pressure was similar in patients with (-13%) and without (-12%) a regression of left ventricular hypertrophy. The mean change in IGF-1 levels with treatment was more pronounced in those patients in whom left ventricular hypertrophy regressed (-25 versus -12%). These results indicate that circulating IGF-1 levels are increased in essential hypertension. Furthermore, there is an association between high IGF-1 levels and left ventricular hypertrophy in hypertensive patients. Our findings suggest that the ability of ACE inhibitors to induce regression of hypertensive cardiac hypertrophy may be related to their ability to normalize IGF-1 and also supports the view that ACE inhibition affects left ventricular mass through pathways other than blood pressure reduction.

Health care delivery for chronic congestive heart failure in the United Kingdom.

Since the United Kingdom has fewer cardiology specialists than other countries, the United Kingdom cardiologist cannot provide direct care for all patients with chronic congestive heart failure (CHF). Most CHF care is provided by general practitioners, physicians or geriatricians. A survey of 100 CHF patients attending a health center revealed that these patients visited their general practitioners 270 times in 1 year, compared with only 34 outpatient visits. The cardiologist mainly provides echocardiography. The accurate diagnosis of mild CHF became imperative with the advent of angiotensin converting enzyme (ACE) inhibitors. Results of a survey showed that although 1.6% of the population are taking diuretics for CHF, only 0.84% of the population have left ventricular systolic dysfunction on echocardiography. An estimated 22 echocardiograms per 1000 population per year are required (10 for structural reasons, three for suspected new CHF, three to identify patients with a low left ventricular ejection fraction and six to identify left ventricular hypertrophy in hypertensive patients). However, district general hospitals in Scotland can only provide 3.3-6 echocardiograms per 1000 population per year. The elderly CHF patient may not receive adequate treatment because of the lack of resources and a dislike of 'overinvestigating' or 'overtreating' the elderly. The benefits of echocardiography and ACE inhibitor therapy for all patients with CHF should be stressed.

Use of the signal-averaged QRS duration for diagnosing left ventricular hypertrophy in hypertensive patients

We analysed the diagnostic performance of the signal-averaged QRS duration for the detection of left ventricular hypertrophy in 100 consecutive outpatients (62 men and 38 women; mean age, 49.8 ± 11.8 years) with essential hypertension and compared the results with some of the currently employed electrocardiographic criteria. Forty-eight healthy subjects (24 men and 24 women; mean age, 46.4 ± 12.1) with normal physical, electrocardiographic and echocardiographic findings served as a control group to derive normal reference values for signal-averaged QRS duration. Twenty-six (26%) hypertensives (22 men and 4 women) had left ventricular hypertrophy echocardiographically defined as a left ventricular mass ≥ 261 g in men and ≥ 172 g in women or left ventricular mass index ≥ 125 g/m 2 in men and ≥ 112 g/m 2 in women. The signal-averaged QRS duration was different in patients with than in those without left ventricular hypertrophy (102.1 ± 10.8 vs. 95.8 ± 8.4 ms; P < 0.01). Also, in the group with left ventricular hypertrophy QRS duration was longer, although not significantly different, in men than in women (103.5 ± 10.7 vs. 94.2 ± 8.8 ms; P n.s.). The correlation between the signal-averaged QRS duration and left ventricular mass was weak but statistically significant in men ( r = 0.34; P < 0.05) in women ( r = 0.30; P < 0.05) and in men and women together ( r = 0.42; P < 0.01). Partition values of filtered QRS duration ≥ 114 ms in men and ≥ 107 ms in women were used to diagnose left ventricular hypertrophy as these values were above the upper limits in our control men and women when 95% confidence intervals were calculated. These criteria were insensitive (12%) but highly specific (99%) for left ventricular hypertrophy. The use of a single threshold value of filtered QRS duration ≥ 111 ms in both sexes combined improved sensitivity modestly (15%) while maintaining a good specificity (95%). Also, we tested the following standard electrocardiographic criteria: the Sokolow-Lyon index, the Romhilt-Estes point score ≥ 4 points and ≥ 5 points, the Cornell voltage criteria, the sum of QRS voltages in all 12 leads > 175 mm, and the QRS duration > 90 ms. Sensitivities ranged from 4% to 58% and specificities from 74% to 99%. To compare the performance for left ventricular hypertrophy of the electrocardiographic criteria we modified, when appropriate, partitions value for test positivity to reach a clinically relevant 95–100% range in specificity. The use of McNemar's test did not show significant differences among sensitivities. Using the same procedure, the 12% sensitivity of the sex-specific signal-averaged QRS duration criteria and the 15% sensitivity of the single QRS duration criterion for both sexes did not significantly differ from each other or from sensitivities of standard electrocardiographic criteria. Therefore, the signal-averaged QRS duration appears to have limitations comparable with standard electrocardiographic criteria in the diagnosis of left ventricular hypertrophy.

Regression of hypertensive myocardial hypertrophy does not affect ultrasonic myocardial reflectivity

Ultrasonic backscatter from the myocardial walls is directly related to the morphometrically or biochemically evaluated collagen content in man, and shows a normal pattern of quantitatively assessed ultrasonic backscatter in hypertensive patients, even in the presence of left ventricular hypertrophy. Whether the pharmacologically induced regression of left ventricular hypertrophy in hypertensive patients is accompanied by a disproportionate increase in relative connective tissue content is not yet known. The objective of the present study was to assess the effects of regression of left ventricular hypertrophy on the quantitatively evaluated myocardial reflectivity in essential hypertensives. We evaluated 19 mild-to-moderate essential hypertensives with echocardiographically assessed left ventricular hypertrophy, before and after 8 months' effective antihypertensive therapy with 20-40 mg enalapril once a day, associated with diuretics or calcium antagonists, or both, in six patients to achieve optimal blood pressure control. Using a modified echo machine developed in the Institute of Clinical Physiology, Pisa, an on-line radio-frequency analysis was performed to obtain quantitative operator-independent measurements of the integrated backscatter signal of the ventricular septum and the posterior wall. The integrated values of the radio-frequency signal from the myocardial walls were normalized for those from the pericardial interface and were expressed as percentages (integrated backscatter index). In comparison with baseline, the treated hypertensives showed significant decreases in mean blood pressure, left ventricular mass index, and septal and posterior wall thickness. However, integrated backscatter index values were similar at baseline and after therapy for both the septum and the posterior wall. Antihypertensive therapy with enalapril does not increase myocardial reflectivity, although it does induce regression of left ventricular hypertrophy. This suggests that, in accord with experimental data, regression of hypertrophy is achieved by enalapril through a proportionate regression of the myocyte and connective tissue components of the myocardium.

Left ventricular hypertrophy in hypertensive patients with different ambulatory monitoring daily pattern

The aim of the present study was to try to identify which parameters of blood pressure (BP) ambulatory monitoring are better related to the presence of left ventricular hypertrophy in hypertensives.

Reproducibility of electrocardiographic criteria for left ventricular hypertrophy in hypertensive patients in general practice.

Before changes in ECG voltage criteria can be accepted as evidence for changes in LVH, the variability of ECG measurements must be known. Here we report on the results of a study, on the variability of electrocardiographic single lead voltage parameters and (voltage) criteria for left ventricular hypertrophy in hypertensive patients in general practice. Two electrocardiograms were recorded, from 64 patients at an interval of 2 min, to measure the minute-to-minute variability. From 77 patients, two electrocardiograms were recorded at an interval of one week to measure the day-to-day variability. The coefficient of variation of voltage parameters for single leads ranged in the day-to-day group from 9.2% in R/I to 42% in T/V1, and the coefficient of variation for voltage combinations in this group ranged from 10.0% for the Sokolow-Lyon criteria to 13.7% for Gubner-Ungerleider criteria. The reclassification percentages in the day-to-day group ranged from 0% for Gubner-Ungerleider to 17% for Minnesota code criteria. A factor analysis showed that studies which use the Romhilt-Estes score, the Sokolow-Lyon or the Minnesota criteria to detect ECG-LVH are not comparable with studies which use the Cornell or Gubner-Ungerleider criteria.

How reliable is the electrocardiogram in detecting left ventricular hypertrophy in hypertension?

This paper assesses the sensitivity and specificity of the electrocardiogram in detecting left ventricular hypertrophy in 75 hypertensive patients. Each patient underwent a 12 lead electrocardiogram and echocardiogram. Left ventricular mass index, using echocardiogram, was calculated according to the Penn convention and left ventricular hypertrophy was assessed by standard electrocardiographic criteria. The electrocardiogram was found to be very specific but insensitive in the detection of left ventricular hypertrophy as compared with the echocardiogram. Other non-voltage dependent markers appeared to have similar reliability. We conclude that the electrocardiogram may be unreliable in the detection of left ventricular hypertrophy in hypertensive patients. Accurate assessment of left ventricular hypertrophy, in these patients should be by echocardiography.

Regression of left ventricular hypertrophy in hypertensive patients: Responses to exercise by antihypertensive treatment.

The effects of various antihypertensive treatments on the echocardiographic and electrocardiographic findings of left ventricular (LV) hypertrophy were studied in 75 patients with essential hypertension. The hemodynamic effects of the therapy during exercise were also compared. LV mass by echocardiogram was significantly reduced by beta-blockade and angiotensin converting enzyme inhibition (ACEI), but only slightly reduced by Ca channel blockade. QRS high voltage criteria of LV hypertrophy by electrocardiogram were reduced by all 3 of these antihypertensive treatments. At submaximal exercise, the pressor responses were attenuated by captopril, but not influenced by metoprolol or nifedipine. The increase in plasma norepinephrine by exercise was significantly suppressed after captopril, but was somewhat augmented after metoprolol or nifedipine. These observations indicate that the responses of hemodynamics and sympathetic nervous activity to exercise are different after the treatment by beta-blocker, Ca channel blocker or ACEI, in spite of the equal antihypertensive effect. However, it is suggested that the regression of LV hypertrophy might be induced by antihypertensive therapy, though the different grade by the individual drug.

Hypertensive Heart Disease

The presence of left ventricular hypertrophy in hypertensive patients has been linked with increased likelihood for developing congestive heart failure, the potential for myocardial ischemia and the inherent risk for sudden death. In this paper we review current knowledge regarding the role of left ventricular hypertrophy in cardiac morbidity and mortality and emphasize the need for further study to explore the efficacy of pharmaceutical agents in reducing cardiac complications of hypertension in high-risk patients.

Left ventricular hypertrophy in hypertensive patients

H ypertension has long been associatetl \vith an increased occurrence of cartliovascular diseases such as stroke, ischemic coronary, artery disease, and congestive heart failure. In addition, it has long been realized that the reduction of elevated blood pressure by effecti\:e antihypertensive therapy helps to reduce the incidence of morbidity and mortality from hypertensive cardiovascular disease in general. The therapeutic goals in the treatment of hypertension therefore include a reduction in blood pressure and attendant hypel.tension-inducetl morbidity and mortality. To accomplish the latter, prevention or reversal of hypertension-induced cardiac structural hypertroph>r is emerging as an important goal of antihypertensive therapy. HyT~ertrophic cardiovascular changes are already evident early in the natural history of hype]*tension and can be used as a prognostic indicator. Specifically, electrocardiographic evidence of left ventricular hvpertrophy is associated with an eightfold increase-in the cardiovascular mortalitv rate and a sixfold increase in the coronary mortality rate ]I]. It is important for clinicians to realize that different antihypertensive agents will have different effects on left ventricular hypertrophy, even though they may effectively reduce blood pressure. In this segment of this supplement, the issue of h:ypertensioninduced left. ventricular hypertrophy is discussed. with a focus on those agents that ina!’ prevent or reverse this serious complication of hypertension. Hypertension affects the heart in several ways. To maintain cardiac output and normal systemic perfusion in the face of a sustained work overload of sufficient magnitude and duration, the heart initially responds by increasing mass and/or volume. This state of cardiac enlargement is due to an increase in the size but not in the number of cardiac myocytes. This compensatory response occurs with the heart utilizing its systolic (Increase in contractility) and/or its diastolic (Starling’s principle) reserves in an attempt to preserve the circulation. Ventricular distention or dilatation will cause an increase in the end diastolic volume. Rut if ventricular dilatation exceeds an optimal value, this initially beneficial response may further exacerbate the load on the heart, and cardiac failure may supervene. The form of the hypertrophic response causing this initial compensatory alteration in cardiac size depends on the type and duration of the jvork load imposed 121. If the heart is burdened by pressure overload, as in hypertension, the overload will manfest as concentric hypertrophy, since the left ventricular mass will increase without chamber enlargement

Left ventricular hypertrophy and ventricular dysrhythmic risk in hypertensive patients: evaluation by programmed electrical stimulation.

Left ventricular hypertrophy in hypertensive patients is associated with an increased prevalence of ventricular arrhythmias. Twelve patients with left ventricular hypertrophy assessed by M-mode echocardiography and 12 without left ventricular hypertrophy underwent an electrophysiological study with programmed electrical stimulation. The patients with left ventricular hypertrophy had a prolonged infranodal conduction time which correlated closely with left ventricular mass (r = 0.71; P less than 0.001). Programmed electrical stimulation initiated more intraventricular re-entry and unsustained ventricular tachycardia in the group with left ventricular hypertrophy than in the control group, although sustained ventricular tachycardia was never induced. We conclude that ventricular vulnerability is increased in hypertensive patients with left ventricular hypertrophy, especially in those who show electrocardiographic evidence of left ventricular hypertrophy.

Reduction of left ventricular hypertrophy in hypertensive patients after treatment with celiprolol

Long-term treatment with celiprolol, a new cardioselective β blocker, significantly reduced blood pressure in 14 patients with essential hypertension (World Health Organization stages I to II). Heart rates remained within the normal range throughout treatment and no significant side effects were observed. In 4 patients, end-systolic septum thickness was measured, and evidence was obtained that the extent of left ventricular hypertrophy was reduced. These findings indicate that celiprolol can be used for the successful long-term treatment of essential hypertension, and that such treatment reduces left ventricular hypertrophy induced by high blood pressure.

Time course of regression of left ventricular hypertrophy in hypertensive patients treated with atenolol.

Regression of left ventricular hypertrophy occurs with a number of antihypertensive drugs, but the time course of this regression has not been defined clearly. We obtained echocardiograms at baseline and serially (on seven occasions) during a 1 year treatment period with the beta-adrenergic receptor inhibitor atenolol in 12 patients with previously untreated essential hypertension. To ensure control of blood pressure in all patients throughout the study, it was necessary to add a thiazide diuretic to the therapy of five patients. Baseline blood pressure was 155/100 mm Hg and fell to 136/84 mm Hg; there was a 20% reduction in heart rate. Posterior and septal wall thicknesses were reduced from 1.16 +/- 0.03 to 1.06 +/- 0.02 cm (p less than .05) and from 1.28 +/- 0.07 to 1.18 +/- 0.06 cm (p less than .05), respectively; this reduction became significant initially at 4 weeks. Left ventricular mass decreased from 144 +/- 9 to 127 +/- 7 g/m2 (p less than .05) and this fall first became statistically significant at 6 months. Significant reduction in electrocardiographic voltages was also seen at 6 months. Therefore, regression of left ventricular hypertrophy with atenolol-induced blood pressure control occurred as early as 4 weeks after starting therapy and was maintained thereafter without apparent compromise of left ventricular systolic function.

Recommendations concerning use of echocardiography in hypertension and general population research.

Use of echocardiography to quantify left ventricular structure and function requires standardization of recording conditions and techniques, accurate machine calibration, and definition of requirements for measurable images. Measurement of left ventricular muscle mass should use M-mode, two-dimensional, or three-dimensional echocardiographic methods that have been anatomically validated to maximize accuracy and comparability of results among studies. Body size and sex influence ventricular muscle mass sufficiently to be taken into account for clinical and research purposes, while age and physical activity are of less certain importance. Echocardiographic studies have clarified the prevalence of left ventricular hypertrophy in hypertensive patients and the effect of blood pressure during normal activity on left ventricular muscle mass, and they have provided data suggesting that left ventricular hypertrophy is a major cardiac risk factor in hypertensive and general populations. Further research is needed to obtain definitive results in these areas, to track the hitherto elusive transition from functionally compensated cardiac hypertrophy to congestive heart failure, and to determine the degree and selectivity of beneficial cardiac effects of antihypertensive treatment. Three-dimensional echocardiographic reconstruction and Doppler measurement of intracardiac blood flow and systemic hemodynamics are likely to extend the usefulness of echocardiography for hypertension and general population research.

Early electrocardiographic diagnosis of left ventricular hypertrophy in hypertensive patients

This study included 25 hypertensive patients with “normal” standard 12-lead scalar electrocardiogram and an equal number of age- and sex-matched controls. We recorded routine twelve leads, posterior chest leads, ensiform lead, right-sided precordial leads, lead CM 5 and oesophageal electrocardiogram at different levels in all individuals. In addition we recorded an unconventional unipolar lead with the chest electrode placed on the thoracic seven spine. We also recorded some unconventional bipolar leads, in each instance using V 5 as the positive electrode and the T 7 spine, or the oesophageal electrode as negative. We observed that the T wave height of 20% or less of R wave amplitude in lead I was highly specific (92%) and sensitive (76%) in detecting early left ventricular hypertrophy in hypertensive patients, with the standard 12-lead electrocardiogram considered “normal” by conventional criteria. The T wave amplitude of 15% or less of the accompanying QRS in lead V 6 was nearly equally diagnostic (specificity 88% and sensitivity 68%). An S wave of 0.3 mV or more in the bipolar lead recorded with the positive electrode at V 5 and the negative electrode on T 7 spine was also highly specific (80%) and sensitive (72%). Isoelectric or inverted T wave in lead V 8, ST segment depression and T wave inversion in lead CM 5 and ST segment depression in the bipolar lead recorded with the positive electrode at the V 5 position and negative electrode at the atrial level of the oesophagus were highly specific (100%) but had a low sensitivity (40, 36, 16, and 28%, respectively). Combined lead V 8 and lead I further improved the sensitivity to 96% without decreasing the specificity.

Diagnosis and Follow up of Left Ventricular Hypertrophy in Hypertensive Patients with Electrocardiography and Echocardiography

Diagnosis and Follow up of Left Ventricular Hypertrophy in Hypertensive Patients with Electrocardiography and Echocardiography

Regression of Left Ventricular Hypertrophy in Hypertensive Patients during a Long-term Treatment with a ??-Receptorblocker

Departments of Cardiology and Sports Medicine, Free University of Berlin, Federal Republic of Germany

Reversal of cardiac hypertrophy by medical treatment.

Reversal of left ventricular hypertrophy in hypertensive patients has been proven to follow effective blood pressure control by some antihypertensive drugs. This reversal does not depend solely on the degree of pressure reduction but is also modulated by other factors including, among others, stability of blood pressure control, degree of cardioadrenergic stimulation, and individual variations due to genetic background and possible age. Regression of left ventricular hypertrophy is most likely to occur when the reduction in arterial pressure and peripheral resistance can be maintained without induced reflex cardiac stimulation. Left ventricular performance at rest was not depressed by the reduction in cardiac mass but remained normal both in absolute terms and in relation to changes in LV end-systolic stress.