Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hypertrophy”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed1984

Clinical significance of left ventricular hypertrophy in dilated cardiomyopathy: an echocardiographic follow-up of 50 patients.

To evaluate the significance of left ventricular (LV) hypertrophy in patients with dilated cardiomyopathy (DCM), 50 patients seen between 1976 and 1983 were studied echocardiographically. We categorized the patients as four groups according to the degree of LV dilatation or hypertrophy. Group consisted of 17 patients with mild to moderate LV dilatation without hypertrophy (LV end-systolic I dimension: Ds less than 60 mm, LV wall thickness at end-systole: WTs less than 15 mm). Group II, 12 with mild to moderate LV dilatation and hypertrophy (Ds less than 60 mm, WTs greater than or equal to 15 mm). Group III, eight with marked LV dilatation and hypertrophy (Ds greater than or equal to 60 mm, WTs greater than or equal to 15 mm), and Group IV, 13 with marked LV dilatation without hypertrophy (Ds greater than or equal to 60 mm, WTs less than 15 mm). Twenty patients had LV hypertrophy and 30 patients were without LV hypertrophy at the start of this study. New York Heart Association functional classes, cardiothoracic ratio and ECG findings at the first study did not show any statistically significant differences among the four groups. During the prospective follow-up of 2.7 years in average, eight patients died of congestive heart failure including five of Group IV, and three of Group I who had progressive LV dilatation. Three patients of Group I, II and III died suddenly. Ambulatory ECGs showed life-threatening ventricular arrhythmias in all 32 patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1980

[Early morphological changes during the development of cardiac hypertrophy (author's transl)].

The development of a cardiac hypertrophy depends on modulation of two parameters, such as the amount of increased work load imposed on the heart and the rapidity with which the work load is applied. A gradual development of cardiac hypertrophy is usually observed in humans; at variance, the induction of cardiac hypertrophy is quite a rapid process in animal experiments. The enlargement of cardiac muscle cells during hypertrophy is due not only to an increased synthesis of contractile proteins but also to an accumulation of other cell constituents parallelly involved in the hypertrophy process. The mechanism whereby new sarcomeres are formed during cardiac hypertrophy is not yet completely clarified. Once the stimulus producing overload is removed, cardiac hypertrophy can regress completely. The possible role of biological regulators in inducing cardiac hypertrophy was also discussed.

Aging↗
PubMed1995

Effect of ouabain in catecholamine-induced cardiac hypertrophy.

Changes in the sensitivity to ouabain of the hypertrophied myocardium were studied in isolated left ventricular trabeculae of rat heart using conventional microelectrode technique, and in anaesthetized rats using limb-lead electrocardiography (ECG). Hypertrophy was induced by administration of 5 mg/kg isoprenaline once daily for 7 days. The age-matched normal control rats received the same volume of 0.9% NaCl solution. The heart weight to body weight ratio increased from 3.23 +/- 0.07 mg/kg to 4.37 +/- 0.12 mg/kg, which means a 35% hypertrophy. The action potential duration at 50% repolarization (APD50) was 25.1 +/- 2.4 ms in normal case and 63.5 +/- 4.6 ms in hypertrophy. The S-T interval of the ECG was 24.9 +/- 1.9 ms in normal rats and 64.4 +/- 3.4 ms in hypertrophy. The toxic effect of ouabain was studied by determining the concentrations of the drug at which arrhythmogenic transient depolarizations (TDs; in microelectrode experiments) or sustained ventricular tachyarrhythmias (VTAs; in ECG experiments) appeared. The dose of ouabain inducing TDs was 345 +/- 25 microM in normal case and 630 +/- 40 microM in hypertrophy. In ECG studies, the dose inducing VTAs was 19.1 +/- 3.6 mg/kg in normal rats and 34.3 +/- 3.1 mg/kg in hypertrophy. The results suggest that catecholamine-induced cardiac hypertrophy damages the membrane-bound Na+, K(+)-ATPase, thus decreasing the number of the ouabain binding sites, which consequently, makes the myocardium membrane more insensitive to ouabain.

Action Potentials↗
PubMed1993

The course of myocardial hypertrophy in hypertrophic cardiomyopathy. Results of a 10-year follow-up.

Sixty-nine patients with hypertrophic cardiomyopathy were followed up for a minimum period of 10 years, with detailed quantitation of myocardial hypertrophy using two-dimensional echocardiography at a two-year interval. The parameters determined included maximum myocardial wall thickness, mean myocardial wall thickness (defined as the arithmetic mean of myocardial wall thickness values measured in ten areas of approximately the same size the LV and septal myocardium had been divided into), and the extent of hypertrophy (percentage of the myocardium affected by hypertrophy). Other echocardiographic parameters as well as clinical, ECG and Holter data were also assessed. Seven patients (10%) showed a gradual increase in mean myocardial wall thickness (associated with an increase in maximum myocardial wall thickness and in the extent of hypertrophy in two). By contrast, a progressive decrease in hypertrophy was observed in six patients (9%). In either case, the observed changes tended to involve areas in segments outside the zone of maximum wall thickness. Generally, the changes in hypertrophy were not related to the development of clinical or Holter manifestations, and were unaffected by verapamil or beta-blocker therapy. There was no death among these patients unlike the five deaths in a group with stationary hypertrophy. Based on their results, the authors conclude that changes in myocardial hypertrophy (regardless of whether there is progression or regression) probably make part of natural variations in the course of the disease, and have no clinical or prognostic implications for the majority of patients.

Adult↗
PubMed1995

[Myocardial hypertrophy and arterial hypertension].

Myocardial hypertrophy in different cardiac diseases is considered to be an adaptive mechanism to the increase of hemodynamic load which might restore to normal radius/wall thickness ratio and consequently to normalize wall stress. However, it has been widely demonstrated that beside the hemodynamic load, other factors contribute to the development of myocardial hypertrophy. It has been shown that in hypertensive patients, functional abnormalities (increased contribution of atrial systole to total diastolic filling, increased isovolumic relaxation period, prolonged diastolic duration, slowed ventricular filling and altered diastolic distensibility) precede the development of myocardial hypertrophy. Thus, in hypertensive patients, sign and symptoms of heart failure could be manifested in absence of myocardial hypertrophy, and might be exclusively due to diastolic dysfunction (with normal systolic function). Systolic function might be involved and compromised late when focal myocardial cell death and fibrosis occur and consequently ¿adequate¿ hypertrophy is shifted to ¿inadequate¿. This evolution is accompanied by morphological and functional changes of the myocardium similar to those encountered in dilated cardiomyopathy. Impairment of systolic function in ¿inadequate¿ hypertrophy is also due to structural changes; altered ratio between sarcomers and mitochondria, increased intercapillary distance, sarcoplasmatic reticulum dysfunction, increase of collagene component with a consequent increment of wall rigidity, hypertrophy of arterial tunica media, which alters coronary flow and coronary reserve. The progression of these morpho-functional abnormalities is a very slow process, in which adaptive mechanism mediated by several enzymes and contractile protein, contribute to maintain myocardial viability. However, over the long course, disseminated focal myocardial cell necrosis and fibrosis, which is an evolving process, is considered to be the main responsible factor for the irreversible myocardial damage and systolic dysfunction in advanced myocardial inadequate hypertrophy.

Cardiomegaly↗
PubMed2003

Angiotensin II and AT1 receptor in hypertrophied ventricles and aortas of sinoaortic-denervated rats.

AIM: Angiotensin II and AT1 receptor are the major effector components of renin-angiotensin system (RAS), and also the main growth-stimulating factors in cardiovascular system. The present study was to observe these two factors in the hypertrophied ventricles and aortas of sinoaortic-denervated rats. METHODS: Rats were examined at 2, 10, and 16 weeks after sinoaortic denervation (SAD). The hypertrophy was evaluated by the ratio of organ weight to body weight. Angiotensin II concentration and AT1 receptor mRNA expression were measured by radioimmunoassay and RT-PCR respectively, using a positive control of candesartan treatment. RESULTS: Aortic hypertrophy existed in 2-, 10-, and 16-week SAD rats, left ventricular hypertrophy in 10- and 16-week SAD rats, and right ventricular hypertrophy in 16-week SAD rats. In all three kinds of examined SAD rats, plasma angiotensin II levels remained unchanged, indicating circulating RAS is at normal level in the chronic phase of SAD. However, cardiovascular tissue RAS was activated, as evidenced by increase of aortic angiotensin II concentrations at 10 and 16 weeks after SAD, and up-regulation of aortic and left ventricular AT1 receptor mRNA expressions at 16 weeks after SAD. CONCLUSION: The activated tissue RAS is secondary to the hypertrophy, and probably involved in the maintenance of cardiovascular hypertrophy following SAD.

Angiotensin II↗
PubMed1996

AAEM minimonograph #46: neurogenic muscle hypertrophy.

Muscle hypertrophy occurs uncommonly in several neurogenic disorders including neuropathies, radiculopathies, spinal muscular atrophy, and post-polio syndrome. Its pathogenesis varies in different circumstances. In the presence of generalized myokymia and neuromyotonia (Isaacs' syndrome), symmetrical hypertrophy appears to be the result of continuous spontaneous electrical stimulation of myofibers and, in some cases, results in type 1 myofiber preponderance. Focal hypertrophy occurring with radiculopathies and mononeuropathies was associated with complex repetitive discharges (CRDs) in approximately half the cases. CRDs may play a role in the pathogenesis of myofiber hypertrophy by continuous myofiber stimulation, but in some cases, with and without CRDs, myofiber hypertrophy may be related to mechanical events. Muscle enlargement seen in old polio appears to involve a significant degree of pseudohypertrophy, although some myofiber hypertrophy occurs. The symmetrical occurrence of hypertrophy in genetically determined disorders, such as spinal muscular atrophy, and hereditary motor and sensory neuropathy types 1 and 2 may have both a genetic and a mechanical basis in addition to pseudohypertrophy in some cases.

Humans↗
PubMed1992

Diastolic left ventricular function after renal transplantation in patients with normal and hypertrophied myocardium.

While diastolic left ventricular (LV) dysfunction is frequent and associated with cardiovascular complications in end-stage renal disease treated with dialysis, controversial information exists on diastolic LV function after renal transplantation. Therefore, Doppler echocardiographic parameters of LV diastolic filling were analyzed in 17 transplanted patients with normal LV mass (< 150 g/m2; mean: 128 +/- 17 g/m2) and 24 transplanted patients with LV hypertrophy (> 150 g/m2; mean: 197 +/- 36 g/m2) and compared with 28 normal controls without and 11 controls with LV hypertrophy. Mean age (normal vs. increased LV mass: 46 +/- 13 vs. 48 +/- 11 years; p = NS) and transplantation duration (60 +/- 35 vs. 50 +/- 37 months; p = NS) were comparable between renal patients, while systolic blood pressure (136 +/- 12 vs. 149 +/- 14 mmHg; p < 0.02) and serum creatinine (1.55 +/- 0.45 vs. 1.98 +/- 0.76 mg/dl; p < 0.05) were higher in patients with than without LV hypertrophy. In transplanted patients with LV hypertrophy, peak early/atrial filling velocity ratios were decreased (1.17 +/- 0.34 vs. 0.94 +/- 0.34; p < 0.05), mean atrial filling fractions were increased (37 +/- 7% vs. 42 +/- 7%; p < 0.05), and isovolumic relaxation periods were prolonged (86 +/- 23 vs. 106 +/- 26 ms; p < 0.02) compared with transplanted patients with normal LV mass. The frequency of pathologic peak early/atrial filling velocity ratios (12 vs. 42%; p < 0.05), atrial filling fractions (12 vs. 25%; p = NS) and isovolumic relaxation periods (6 vs. 29%; p = NS) was higher in transplanted patients with than without LV hypertrophy. Individual ratios of peak early/atrial filling velocity were inversely correlated with age in transplanted patients with normal LV mass (p < 0.002), and atrial filling fractions were correlated with LV mass index in transplanted patients with LV hypertrophy (p < 0.01). Diastolic LV function was comparable in both groups of transplanted patients with their corresponding non-renal controls. It is concluded that, in transplanted patients, diastolic LV filling is comparable to nonrenal controls; it is age-dependent in patients with normal LV mass and mass-dependent in those with LV hypertrophy.

Aging↗
PubMed1988

Prognostic implications of renal hypertrophy in diabetes mellitus.

Early in the course of type 1 diabetes mellitus, hypertrophy of the kidney is a consistent finding that is easily diagnosed using current noninvasive methods, especially ultrasonography. Renal functional changes occur in association with hypertrophy, most notably glomerular hyperfiltration. The structural counterpart of this functional change is an early increase in capillary filtration surface area. In most forms of nondiabetic renal hypertrophy, kidney size is closely linked to GFR. In contrast, in diabetes, persistence of hypertrophy after the clinical onset of overt kidney disease (microalbuminuria, hypertension, decreased GFR, etc.) suggests that sustained release of one or more growth factors may continue even after kidney function declines. The fact that growth factors can act in both an autocrine and paracrine fashion raises the possibility that the local effects of such substances may act as local mediators of kidney growth. Failure of renal hypertrophy to reverse following strict glycemic control for a few months may turn out to be an important prognostic indicator of future progression of the renal disease, but this remains to be established. Prospective studies of kidney size in patients with newly diagnosed type 1 diabetes, using accurate noninvasive methods, may be helpful in establishing whether irreversible ("autonomous") hypertrophy of the kidney is indeed a useful prognostic indicator. As therapies are developed that target the different microvascular complications of diabetes (retinopathy, nephropathy, neuropathy), a noninvasive estimation of kidney size may be a cost-effective method of predicting ultimate renal involvement. Since microalbuminuria occurs relatively late in the disease process, early and persistent hypertrophy of the kidney may become a useful prognostic test in the earliest stages of the disease.

Animals↗
PubMed1994

Reduced calcium current density in single myocytes isolated from hypertrophied failing guinea pig hearts.

The present study explored the possibility that an alteration in the transmembrane calcium current (ICa), through its ability to modulate Ca2+ release from the sarcoplasmic reticulum, could contribute to the depressed peak [Ca2+]i we previously observed in hypertrophied failing myocardium. Whole-cell patch clamp was used to measure ICa in single guinea pig ventricular myocytes isolated from hearts of normal guinea pigs and from guinea pig hearts in which hypertrophy and failure were induced by gradually developing left ventricular pressure overload subsequent to ascending aortic banding of young animals. Membrane capacitance (Cm) was significantly greater. and ICa, normalized for Cm, was significantly lower in myocytes from hypertrophied failing hearts. Myocytes from hypertrophied failing hearts did not differ significantly from normal myocytes in terms of the voltage-dependence of the activation variable (d) of ICa (except at -30 mV), the time course of removal of inactivation of ICa, and the time constant of decay of ICa. Measurement of the voltage dependence of the inactivation variable (f) of ICa showed that significantly more steady-state inactivation was present at 0, -10, and -20 mV in myocytes from hypertrophied failing hearts. Multiple regression analysis of all data indicated that ICa density decreased with increasing myocyte membrane area (as reflected by Cm) irrespective of any specific effects of hypertrophy and heart failure. We conclude that ICa, normalized for Cm, is significantly reduced in myocytes isolated from hypertrophied failing hearts, probably by a process associated with increased cell size, per se.

Animals↗
PubMed2000

Regression of chronic L -NAME-treatment-induced left ventricular hypertrophy: effect of captopril.

Long-term administration of N(G)-nitro- L -arginine methyl ester (L -NAME) induces development of NO-deficient hypertension and left ventricular (LV) hypertrophy. In this work, we examined the effect of spontaneous and captopril-induced recovery on LV hypertrophy and protein composition in rats with developed L -NAME-induced hypertension. Four groups of rats were investigated: control L -NAME 40 mg/kg/day for 4 weeks (L -NAME) L -NAME 40 mg/kg/day for 4 weeks followed by 3-week spontaneous recovery (L -NAME+R) L -NAME 40 mg/kg/day for 4 weeks followed by 3 weeks of captopril treatment at a dose of 100 mg/kg/day (L -NAME+C). LV hypertrophy in the L -NAME group was associated with an increase in content and concentration of left ventricular DNA and RNA, concentration of metabolic proteins (MP) and soluble collagenous proteins (SCP). Spontaneous recovery period reduced the hypertension, without regression of LV hypertrophy. Left ventricular DNA and RNA content were increased in the L -NAME+R group. In this group, concentrations of MP, contractile proteins (CP), and collagenous proteins did not differ from those in the L -NAME group. Captopril treatment caused total regression of hypertension and LV hypertrophy and decreased both content and concentration of DNA and RNA, as well as the contents of MP, CP and SCP v the L -NAME group. However, after captopril treatment, concentration of collagenous and non-collagenous protein fractions remained increased v control. We conclude that spontaneous regression of L -NAME-induced hypertension is not associated with regression of LV hypertrophy. LV hypertrophy was regressed only in captopril-treated animals.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Increased sodium-calcium exchange current in right ventricular cell hypertrophy induced by simulated high altitude in adult rats.

Ventricular hypertrophy is associated with an increase in action potential (AP) duration which is potentially arrhythmogenic. The implication of the Na-Ca exchange current (I(Na-Ca)) in the lengthening of the AP is controversial. The role of this current in the increased duration of the low plateau of the AP in hypertrophied adult rat ventricular myocytes by simulated chronic high-altitude exposure ( approximately 4500 m) was evaluated. Electrophysiological experiments were carried out on isolated right ventricular myocytes from exposed and control rats with the perforated patch or the conventional whole-cell technique in current or in voltage clamp condition. With the two techniques, a significant increase of the low plateau duration was observed in hypertrophied myocytes as compared to controls. The low plateau in hypertrophied myocytes was depressed when Na was replaced by Li and was no longer recorded when intracellular Ca was buffered with EGTA. Inward tail currents, evoked either on repolarization to -80 mV following a depolarizing pulse to +10 mV or by interrupted AP technique, were greater in hypertrophied than in control myocytes and were abolished when Na was replaced by Li or when intracellular Ca was buffered with EGTA, indicating an increased Na-Ca exchange activity. The Li-sensitive current-voltage curves, obtained by a voltage clamp ramp protocol with an intracellular calcium buffered solution, were not significantly different in both hypertrophied and control myocytes, suggesting no modification in the density of the Na-Ca exchange protein. This was corroborated by the lack of difference in NCX1 mRNA levels between right ventricles from control and exposed rats. We conclude that increased duration of the low plateau of rat ventricular AP in altitude cardiac hypertrophy may be attributed to an increase of the inward I(Na-Ca). This augmented I(Na-Ca)may result from a modification in the intracellular Ca homeostasis.

Action Potentials↗
PubMed1989

Effect of hindlimb immobilization and recovery on compensatory hypertrophied rat plantaris muscle.

Compensatory hypertrophy of the rat plantaris muscle (PLT) was induced by ipsilateral gastrocnemius muscle ablation. Following 8 weeks (wks) of hypertrophy, hindlimbs were cast immobilized (HI) for 4 weeks after which weight bearing was unrestricted for 8 wks (recovery). Compensatory hypertrophy increased PLT wet weight/body weight ratio (83%), muscle fiber cross-sectional areas (1.5 to 2 fold), and the percent of slow oxidative (%SO) fibers (2 fold) in the experimental compared to the contralateral sham control muscle. PLT protein content and maximal activities of phosphofructokinase (PFK), mitochondrial glycerol phosphate dehydrogenase, and succinate dehydrogenase were unaltered with muscle hypertrophy. HI produced significant decreases in PFK activity (50%) and muscle fiber cross-sectional areas (50%) but did not significantly change the histochemical myofibrillar ATPase profile. Following remobilization, muscle weight/body weight ratio and maximal enzyme activities recovered to that of aged matched controls. Muscle fiber areas returned to pre-immobilization sizes but were approximately 25% smaller than aged matched control hypertrophy muscles. The %SO fibers in the hypertrophied muscle remained higher than controls but did not return to pre-immobilization values. These results indicate that biochemical and histochemical characteristics of hypertrophied rat PLT recover from HI during 8 wks of normal weight bearing similar to that of normal control muscle. However, the recovery time period was insufficient to allow complete compensation of fiber size to that of the age-matched control animals.

Animals↗
PubMed1995

Effect of octreotide and insulin on manifest renal and glomerular hypertrophy and urinary albumin excretion in long-term experimental diabetes in rats.

Treatment of diabetic rats with octreotide can inhibit early diabetic renal hypertrophy. Octreotide administration for 6 months from the day of diabetes induction inhibits renal hypertrophy and diminishes increase in urinary albumin excretion. To investigate the effect of octreotide on manifest diabetic renal changes, octreotide treatment was given for 3 weeks after an untreated diabetic period of 3 or 6 months. In addition, following 6 months of diabetes, a group of diabetic rats was treated with insulin for 3 weeks. Renal and glomerular hypertrophy, and increased urinary albumin excretion were observed in diabetic rats compared to non-diabetic control rats from 3 months and throughout the study period. Octreotide treatment did not affect body weight, food intake, blood glucose or serum fructosamine levels. We observed no effect of octreotide treatment on renal and glomerular hypertrophy or urinary albumin excretion compared to placebo-treated diabetic rats. Insulin treatment for 3 weeks after 6 months of untreated diabetes normalized blood glucose and serum fructosamine levels, and furthermore renal hypertrophy was significantly diminished compared to the placebo-treated diabetic rats. However, insulin treatment had no effect on glomerular hypertrophy or urinary albumin excretion. In conclusion, octreotide treatment for 3 weeks following an untreated diabetic period of 3 or 6 months is unable to reduce the increased renal and glomerular volume or urinary albumin excretion. However, insulin treatment for 3 weeks with induction of euglycaemia diminishes the renal hypertrophy but has no effect on glomerular volume or urinary albumin excretion.

Albuminuria↗
PubMed1995

Association between left ventricular hypertrophy and erythrocyte sodium-lithium exchange in normotensive subjects with and without NIDDM.

The determinants of left ventricular mass in normal control subjects and subjects with non-insulin-dependent diabetes (NIDDM) are ill-defined. We therefore recorded M-mode and pulsed Doppler echocardiograms and 24-h ambulatory blood pressure in 57 normotensive subjects, 34 with NIDDM and 23 matched non-diabetic control subjects. Measurements of erythrocyte sodium-lithium counter-transport, plasma angiotensin II, plasma and platelet catecholamines and fasting plasma insulin were also made. Six control subjects (26%) and 15 diabetic subjects (44%) had some degree of left ventricular hypertrophy. Subjects with left ventricular hypertrophy (n = 21) had an elevated mean rate of sodium-lithium countertransport (0.40 +/- 0.13 vs 0.31 +/- 0.09 mmol.l-1.h-1; p < 0.01), parallel differences being observed in both the diabetic and control groups. Twelve of the subjects with left ventricular hypertrophy (57%) had elevated rates of sodium-lithium counter-transport compared to only seven (19%) of those without (p < 0.05). There was no consistent difference between those with and without left ventricular hypertrophy in any other clinical or biochemical variable. Multivariate analysis, with the presence or absence of left ventricular hypertrophy as the dependent variable, demonstrated that the maximal rate of sodium-lithium countertransport was the only variable that independently contributed to left ventricular hypertrophy (partial r = 0.35; F1.55 = 7.74; p = 0.007). This study demonstrates for the first time an association between left ventricular hypertrophy and erythrocyte membrane cation transport that is independent of hypertension, is present in both diabetic and non-diabetic groups, and may represent a link between elevated rates of membrane sodium transport and cardiovascular risk.

Adult↗
PubMed1994

Ventricular dysrhythmias, left ventricular hypertrophy, and sudden death.

Left ventricular hypertrophy has been documented to be a powerful risk factor for sudden death, acute myocardial infarction, and other cardiovascular morbidity and mortality. The major determinant of left ventricular mass is the hemodynamic burden. However, the hypertrophic process is modified by demographic parameters (age, sex, race), nutritional parameters (salt intake, alcohol, obesity), and neuroendocrine factors (angiotensin, catecholamines, growth hormones, etc.). Ventricular ectopy and more serious arrhythmias are commonly seen in patients with left ventricular hypertrophy. Specific antihypertensive therapy will reduce left ventricular hypertrophy, although not all antihypertensive drugs are equipotent in this regard. A reduction in left ventricular hypertrophy has been shown to diminish left-ventricular-hypertrophy-associated arrhythmias. However, it remains to be shown that patients with left ventricular hypertrophy and ventricular ectopy are at a higher risk of sudden death than those without ventricular ectopy and that the reduction of left-ventricular-hypertrophy-associated ventricular ectopy indeed confers a clinical benefit that exceeds the one from the reduction in arterial pressure alone.

Antihypertensive Agents↗
PubMed1993

Decreased mid-to-late diastolic decay of diastolic coronary artery flow velocity in pressure-overloaded left ventricular hypertrophy.

This study was carried out to investigate the characteristics of coronary arterial flow in left ventricular hypertrophy secondary to systemic hypertension. The blood velocities in the left anterior descending coronary artery (LAD) were measured by a No. 3F 20 MHz Doppler catheter in 23 hypertensive patients with left ventricular hypertrophy (systolic/diastolic pressure: 181 +/- 15/100 +/- 4 mmHg) and 13 patients with atypical chest pain, but without left ventricular hypertrophy and any abnormal hemodynamic findings. All patients had normal coronary arteriograms. The LAD blood velocity waveforms in pressure overloaded left ventricular hypertrophy were characterized by both a decreased mid-to-late diastolic deceleration rate (delta V/delta T) and a normalized value of delta V/delta T by peak diastolic velocity [delta V/(delta T.Vpeak)], as well as delayed early diastolic inflow (time for diastolic rise; TDR). The values of the delta V/(delta T.Vpeak) in the patients with hypertensive left ventricular hypertrophy and in the normotensive controls were 1.26 +/- 0.61 and 3.03 +/- 1.18/s, respectively (P < 0.001). The TDR was 145 +/- 56 and 66 +/- 15 ms (P < 0.001). In patients with hypertensive left ventricular hypertrophy, the delta V/(delta T.Vpeak) correlated well with the degree of hypertrophy (r = 0.75, P < 0.01) and with the TDR (r = 0.82, P < 0.01). The coronary flow reserve, calculated from the ratio of the diastolic mean velocity after intracoronary injection of papaverine to the resting flow velocity increased with the delta V/(delta T.Vpeak) (r = 0.68, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Importance of cardiac, but not vascular, hypertrophy in the cardiac baroreflex deficit in spontaneously hypertensive and stroke-prone rats.

In the present study, we examined whether antihypertensive treatment of young and adult hypertensive rats with the angiotensin-converting enzyme (ACE) inhibitor perindopril could restore the baroreflex vagal deficit and whether this was related to prevention of cardiac or vascular hypertrophy. Spontaneously hypertensive (SHR), stroke-prone spontaneously hypertensive (SHR-SP), and Wistar-Kyoto (WKY) rats were untreated or treated with perindopril (3 mg/kg/day) in the drinking water from 4-9 and from 14-20 weeks of age. Steady-state sigmoidal mean arterial pressure (MAP)-heart rate (HR) reflex curves were obtained in the conscious rats by the injection of pressor and depressor agents before and after atenolol (vagal component). Increased left ventricle to bodyweight ratio (LV/BW) indicated cardiac hypertrophy. After ganglion blockade, the minimum MAP produced by nitroprusside and the maximum produced by methoxamine were used as indications of vascular hypertrophy. Perindopril treatment reduced cardiac and vascular hypertrophy to different extents in SHR and SHR-SP. The 4-9 and 14-20 week treatments reduced MAP and both minimum and maximum blood pressure of the SHR to the levels of the untreated WKY. However, only in the older animals was LV/BW restored. In the SHR-SP, early treatment had a much greater effect on vascular hypertrophy than on LV/BW. The reverse occurred for the 14-20 week animals. In untreated hypertensive animals the baroreflex curves were shifted to the right with reduced vagal HR range. Perindopril treatment shifted the baroreflex curves back towards the WKY curves. Vagal HR range was strongly correlated with the LV/BW, whereas vagal HR range was less well related to the level of vascular hypertrophy or blood pressure. These results suggest that antihypertensive treatment can restore cardiac baroreflex function and that it is related to the reduction in cardiac hypertrophy. Although the mechanism of this relationship remains to be elucidated, these findings suggest that cardiac vagal afferents may be important.

Angiotensin-Converting Enzyme Inhibitors↗