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PubMed2004

[Expression of chemokine-like factor 2(CKLF2) mRNA in rat myocardium with hypertrophy].

OBJECTIVE: To investigate the expression of CKLF2 mRNA in the rat myocardium with hypertrophy. METHODS: Rat abdominal aorta was constricted by operation to make myocardium hypertrophy in the hypertrophy group and the control group was subjected to the sham-operation. The CKLF2 mRNA expressions were tested by competitive polymerase chain reaction (CPCR). RESULTS: Compared to the control-group, the expression of CKLF2 mRNA of hypertrophy-group significantly increased on the 17th day after operation, and decreased to the control level on the 45th day. CONCLUSION: The expression of rCKLF2 mRNA in rat myocardium with hypertrophy significantly increased in early days of hypertrophy.

Animals↗
PubMed2004

[Aminoguanidine prevents peroxynitrite production and cardiac hypertrophy in streptozotocin-induced diabetic rats].

UNLABELLED: The effect and possible mechanisms of action of aminoguanidine (a preferential iNOS inhibitor) has been studied on cardiovascular damages and overproduction of reactive nitrogen species in streptozotocin-induced diabetic rats. MATERIALS AND METHODS: 40 rats were divided into five groups (control and diabetic, with or without aminoguanidine treatment, diabetic with insulin treatment) and oxidative stress parameters were examined. Tissue nitric oxide levels were determined by EPR spectroscopy, while peroxynitrite generation by a chemiluminescence method. Cardiac hypertrophy, blood metabolic parameters (blood glucose, HbA1c, fructosamine), as well as tissue protein carbonyl levels were also determined. RESULTS: Diabetic animals showed increased nitric oxide and peroxynitrite generation in the aorta along with a significant hypertrophy and protein carbonylation of the cardiac tissue. Both aminoguanidine and insulin treatment suppressed high levels of nitric oxide and peroxynitrite in the vasculature, but only aminoguanidine was able to prevent hypertrophic alterations and to reduce protein carbonylation in the heart. CONCLUSIONS: The results show that (1) aminoguanidine reduces nitric oxide production and prevents cardiac hypertrophy, (2) insulin therapy improves carbohydrate metabolism, reduces nitrosative stress but has no effect on cardiac hypertrophy. Cardiac hypertrophy in diabetes is strongly correlated with non-enzymatic glycation. Aminoguanidine prevented hypertrophy by blocking the formation of advanced glycation end products rather than via other mechanisms.

Animals↗
PubMed1992

[Hypertrophy of neonates in diabetic mothers and their long-term prognosis].

Hundred and seventy five infants of diabetic mother born and followed up carefully in the Institute for the Care of Mother and Child were examined at a mean age of 20.75 +/- 4.08 years. The purpose of the investigation was to assess the relationship of hypertrophy of neonates of diabetic mothers to other deviations in neonates and their long-term prognosis. In neonates with a marked degree of hypertrophy the authors recorded significantly more frequently hypoglycaemia, early asphyctic syndrome, impaired respiration and neurological symptoms. Children born as hypertrophic developed equally frequently diabetes (8.7%) as children of diabetic mothers who did not develop hypertrophy (8.0%). Abnormal glucose tolerance was recorded in those with hypertrophy in 6.6%, in the group without hypertrophy in 5.0%. As compared with the offspring of healthy mothers, they suffered significantly more frequently from higher blood sugar levels and higher insulinaemia (sigma C ad sigma I) during the oGTT. The body weight expressed as BMI and systolic blood pressure were also higher than in the control group. None of the investigated indicators in adult age was associated with body weight and the degree of hypertrophy. The development of diabetes is determined more by genetic factors.

Adult↗
PubMed1991

Effects of mild cardiac hypertrophy, induced by volume overload in turkeys, on myocardial sarcoplasmic reticulum calcium-pump and calcium-channel activities and on the creatine kinase system.

Recent studies indicate that in animals with marked cardiac hypertrophy, there is depressed function of Ca2+ sequestration by myocardial sarcoplasmic reticulum (SR) because of down regulation of the Ca(2+)-ATPase gene. However, in several animal models we have observed enhancement of myocardial Ca2+ sequestration in response to chronic cardiac stimulation. We tested the hypothesis that in animals with mild cardiac hypertrophy, there is enhanced Ca(2+)-cycling activity by the SR Ca2+ pump and Ca(2+)-release channel. Because creatine kinase activity is consistently decreased in cardiomyopathy, we also determined whether enhanced Ca2+ cycling was accompanied by down regulation or inhibition of the creatine kinase system. Mild cardiac hypertrophy was induced by volume overload; 2% salt was added to the diet of 2-week-old turkey poults for 4 weeks. Compared with age-matched controls, volume overload resulted in 14.3% increase in heart weight and 21.5% increase in heart-to-body weight ratios. The hypertrophied heart had approximately 20% increased activities of the SR Ca2+ pump and the SR Ca2+ channel. Net Ca2+ transport was increased by 16.5%. Compared with controls and in contrast to several other myocardial enzymes, creatine kinase activity was diminished in the hypertrophied hearts by 23% and creatine content was decreased by 8%. Differences between groups were not detected for lactate dehydrogenase, aspartate transaminase, and alanine transaminase. We concluded that an early adaptation of the myocardium undergoing hypertrophy in compensatory response to functional overload is an enhancement of Ca2+ cycling activity by the Ca2+ pump and Ca2+ channel of the SR.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Protective effects of calcium antagonists on energy and substrate metabolism during ischemia and reperfusion in hypertensive myocardial hypertrophy.

The aim of the present study was to define the protective effects of verapamil and nifedipine on mechanical performance and energy and substrate metabolism of the postischemically reperfused myocardium in a chronic pressure overload cardiac hypertrophy model. The isolated beating rat heart preparation was used and left ventricular pressures and high-energy phosphates were continuously monitored during 30 min of global ischemia and reperfusion, respectively. Recovery of mechanical performance and high-energy phosphate and sugar monophosphate metabolism was significantly impaired in untreated hypertrophied hearts compared with normal control hearts and hypertrophied hearts treated with calcium antagonists. In hypertrophied hearts with chronic verapamil treatment, recovery was significantly improved compared to acute verapamil treatment, nifedipine treatment, and normal control hearts. Thus, verapamil and nifedipine exerted a protective effect on the postischemic recovery of the hypertrophied myocardium that was most prominent following long-term pretreatment with verapamil. Prolonged maintenance of adequate plasma levels and tissue distribution of calcium antagonists before an ischemic event may improve the postischemic prognosis in the presence of pressure-induced myocardial hypertrophy.

Adenosine Triphosphate↗
PubMed1991

[The echocardiographic evolution of left ventricular hypertrophy in treated hypertensive patients. A long-term follow-up].

In order to study the possible regressive changes of left ventricular hypertrophy in treated hypertensive patients and to correlate them either with the drugs they received and/or the blood pressure reduction obtained, a long-term (6 years) echocardiographic follow-up study was performed in 61 patients. B and M mode echocardiographic septum and posterior wall thickness and left ventricular mass index were measured yearly and the type of ventricular hypertrophy, asymmetric septal or concentric (symmetric), were compared before and after the follow-up. Sixteen patients received only diuretics; 14, only propranolol, and associated therapy was used in the remaining 31 patients. Average blood pressure was significantly reduced in the whole group of patients, but, individually, 30 of them achieved normal levels for the diastolic (90 mmHg), remaining it over this value in the other, although all of them experienced an average reduction 10 mmHg with therapy. Those patients with concentric hypertrophy at entry showed a significant septal, posterior wall thickness and total ventricular mass reduction during the follow-up, those with initial asymmetric septal hypertrophy, a significant septal thickness and ventricular mass reduction, and those without hypertrophy on admission, showed an average paradoxical increase in septal thickness. We conclude that left ventricular hypertrophy disappeared or decreased in 48% of the patients and that treatment seems to prevent its progression or development in the 43% of all patients. The regressive or favorable changes were significantly more frequent among patients with normal blood pressure after treatment as well as among patients treated only with propranolol in comparison to those treated only with diuretics.

Antihypertensive Agents↗
PubMed1991

[Evaluation of pulmonary venous flow pattern in hypertrophied and dilated hearts: a study with transesophageal pulsed Doppler echocardiography].

In order to evaluate the clinical significance of pulmonary venous flow (PVF) pattern, transesophageal pulsed Doppler echocardiography (TEE) was performed in 25 patients with hypertrophied heart (all with hypertrophic cardiomyopathy), 15 patients with dilated heart (10 with old myocardial infarction and 5 with dilated cardiomyopathy) and 10 normal controls. Parameters obtained from the PVF pattern were compared with those of transmitral flow (MVF) pattern, % fractional shortening (%FS) of left ventricle (LV) and amplitude of mitral anular motion (MAM) during a cardiac cycle. Results were as follows: 1. PVF pattern in cases of sinus rhythm was divided into four components, atrial systolic backward flow (PVA), ventricular systolic (PVS1, PVS2) and diastolic (PVD) forward flows. 2. In patients with dilated heart, peak velocities of PVS1 and PVS2 were markedly decreased compared with those of hypertrophied and normal hearts. 3. Peak velocity of PVD in hypertrophied and dilated hearts was significantly decreased compared with that of normal controls, and PV-D/S (ratio of peak velocity of PVD to PVS2) was significantly lower in hypertrophied heart than in normal controls. 4. Time interval from the first heart sound to the peak of PVS2 (TS) was significantly longer in dilated heart, and time interval from the second heart sound to the peak of PVD (TD) was longer in hypertrophied heart than in the other two groups. 5. MAM and %FS of dilated heart were significantly lower than those in normal and hypertrophied hearts, and peak velocity of PVS2 in dilated heart group correlated well with MAM or %FS. 6. There were significant correlations among the diastolic parameters from PVD of PVF (peak velocity of PVD, PV-D/S) and early diastolic wave (D) of MVF (peak velocity, deceleration time and deceleration of rapid filling). 7. In a case of hypertrophic cardiomyopathy with mid-diastolic wave of MVF, distinct forward wave was observed after PVD of PVF, and this wave coincided in timing with the mid-diastolic wave of MVF. 8. In a case of extensive myocardial infarction with the development of severe LV dysfunction and with "normalized" pattern of MVF, peak velocities of PVD and PVA were markedly increased, and that of PVS2 was decreased. However, the peak velocities of PVD and PVA were decreased, and that of PVS2 was increased with the fair improvement of LV dysfunction and with the compensatory augmentation of atrial contraction wave (A) of MVF.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1990

[Angiotensin-converting-enzyme inhibitor and heart hypertrophy].

There is evidence from experiments in animals, biological and molecularbiological investigations, that extra-renal renin-angiotensin systems may have important implications in the pathogenesis of various diseases, in particular in regard to the development of hypertrophy in smooth muscle cells of blood vessels and in the myocardium. Thus, it is getting more likely, that angiotensin II is an endogenous growth factor. We have recently shown, in an animal model of left ventricular hypertrophy (aortic stenosis due to a silver clip on the aorta ascendens), that chronic application of an ACE-inhibitor results in a nearly complete regression of left ventricular hypertrophy even under the conditions of an unaltered afterload. The extent of the regression of left ventricular hypertrophy was not statistically different from animals in which the regression of hypertrophy was achieved by removal of the clip. According to these results, we demonstrated for the first time, that the renin-angiotensin system plays a major role in the maintenance of left ventricular hypertrophy and that after the inhibition of the system, a considerable regression of left ventricular mass can be achieved which is independent from hemodynamic factors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

The effect of cardiac hypertrophy on changes in cytosolic free calcium concentration during ischemia.

Chronic ventricular hypertrophy caused by pressure overload is a common associated risk factor in congenital cardiac surgery. Because calcium controls contractile protein interaction, we postulated that inducing ventricular hypertrophy from birth alters the way myocytes are able to regulate free cytosolic calcium (Cai) during ischemia. In this study we measured Cai with a recently developed intracellular fluorescent probe trapped inside myocytes by deesterification. The probe shifts its fluorescence spectra (from 380 to 340 nm; fluorescence measured at 510 nm) when it binds to calcium in direct relation to Cai. We studied the effects of ischemia at 37 degrees C (up to 50 minutes) on Cai in newborn (3 to 5 days), adult control (2 to 4 months old), and hypertrophied (2 months old; aortic banding done at 10 days) isolated retroperfused rabbit hearts loaded with Fura-2. In a separate group of hearts (n = 6 per group) we measured isovolumic peak developed pressure with an intracavity balloon in hearts subjected to 30 minutes of ischemia at 37 degrees C and 30 minutes of reperfusion. The recovery of peak developed pressure (percent of preischemic control) was 101% +/- 6% in control, 85% +/- 4% (p less than 0.05 vs control) in newborn, and 67% +/- 7% (p less than 0.05 vs control) in hypertrophied hearts. Cai-dependent fluorescence rose to 160% +/- 30% of preischemic baseline levels by 30 minutes of ischemia in control versus a decline to 55% +/- 7% (p less than 0.05 vs control) in newborn and 51% +/- 2% (p less than 0.05 vs control) in hypertrophied hearts by 30 minutes of ischemia. We conclude that hypertrophied and newborn hearts have a lower Cai during ischemia compared with adult hearts, and this is associated with a worse recovery of cardiac function. The lower Cai may be the result of irreversible binding of calcium to contractile proteins.

Animals↗
PubMed1990

Deferoxamine fails to improve postischemic cardiac function in hypertrophied hearts.

Myocardial hypertrophy is a well-recognized risk factor in congenital cardiac surgery. Hypertrophied hearts have been demonstrated to have an increased vulnerability to ischemia/reperfusion injury. We studied the effects of the iron chelator and hydroxyl radical scavenger deferoxamine given during early reperfusion in a model of isolated retroperfused rabbit hearts made hypertrophic by aortic banding early in life (1 week of age). The rabbits were studied at 6-8 weeks of age, and the hearts were subjected to 30 minutes of 37 degrees C ischemia followed by 30 minutes of reperfusion. Postischemic recovery of isovolumic developed pressure was measured by using an intracavitary balloon in both the untreated (n = 6) and the deferoxamine-treated (n = 6) groups and compared with normal age-matched controls. Deferoxamine (50 mumol/kg) was given to one group with the hypertrophied hearts during the first 10 minutes of reperfusion. The left ventricular weight/body weight ratio in the hypertrophied hearts was 2.9 +/- 0.4 x 10(-3) (n = 14) versus 2.0 +/- 0.1 x 10(-3) in the age-matched controls (p less than 0.05). Postischemic peak developed pressure recovered to 102 +/- 6% of the preischemic value in the normal hearts after 30 minutes of reperfusion compared with 75 +/- 5% for the untreated and 71 +/- 4% for the deferoxamine-treated hearts (p less than 0.05 vs. control). We conclude that chronic hypertrophy from early in life leads to increased susceptibility to ischemia and that the iron chelator deferoxamine is not effective in preventing the injury of reperfusion in hypertrophied hearts.

Animals↗
PubMed1990

[Antihypertensive treatment and remission of left ventricular hypertrophy. Critical study].

Left ventricular hypertrophy which is the adaptive mechanism of the heart to hypertension may become a cardiovascular risk factor independent of the hypertension which induced it: the regression of left ventricular hypertrophy therefore constitutes one of the medium-term objectives of antihypertensive therapy. Some antihypertensive drugs make the left ventricular hypertrophy regress early and permanently: methyldopa, betablockers, converting enzyme inhibitors, calcium antagonists. The reduction of myocardial mass is slight or debatable with diuretics and absent or inconstant with vasodilator therapy. The regression of left ventricular hypertrophy in hypertension raises several problems: the reliability of methods of measurement; inter-individual and inter-drug variations; the beneficial nature of this regression; the preventive effect of regression of left ventricular hypertrophy on cardiovascular complications. In the light of recent trials, early treatment of hypertension may prevent the development of left ventricular hypertrophy.

Animals↗
PubMed1990

Outward currents in hypertrophied feline ventricular myocytes.

In the present study we have characterized the inward rectifying K current, I(K1), and the delayed rectifying outward current, I(X1), in single feline ventricular myocytes isolated from normal cats and animals with experimentally induced RVH. The ionic currents described in this study share many characteristics with the ionic currents first observed in multicellular preparations, but differ from them in several important respects, most notably the presence of a negative slope region in the background (IK1) current: voltage relationship and the relative insensitivity of I(X1) to block by traditional K channel blockers. These findings are similar to those reported for these currents in other preparations of single ventricular or Purkinje myocytes. The present study also demonstrates that there are several abnormalities of I(K1) and I(X1) in hypertrophied myocardium. The magnitude of I(K1) is larger in hypertrophy myocytes, while the magnitude of I(X1) is reduced. I(X1) showed steeper rectification, slower activation, and more rapid deactivation in hypertrophy myocytes, abnormalities which may contribute to the prolonged AP duration of hypertrophied myocardium. These findings, in addition to our previous report on alterations of the slow inward Ca current in hypertrophied myocardium, add to our understanding of the electrophysiologic derangements induced by pressure overload cardiac hypertrophy.

Action Potentials↗
PubMedDate not supplied

Capillary and pre-capillary coronary vascular growth during left ventricular hypertrophy.

An inadequate vascular growth during pressure-overload cardiac hypertrophy involves both pre-capillary and capillary vessels. With the development of hypertrophy in spontaneously hypertensive rats (SHR) coronary reserve declines as indicated by increases in minimal coronary vascular resistance (MCVR). Capillary numerical density, surface density, and volume density also decline. However, after hypertrophy becomes stabilized late in life these parameters return to normal. That elevated blood pressure plays a major role in the decrement in coronary reserve was demonstrated by treating prehypertensive SHR with hydralazine which prevented hypertension but not cardiac hypertrophy. In these animals capillary density remained depressed but coronary reserve was normal. Capillary growth in SHR was, however, stimulated by exercise training even though blood pressure and cardiac hypertrophy were unaffected. Studies on thyroxine-induced cardiac hypertrophy provided evidence of a substantial angiogenesis. In this model coronary reserve is normal or slightly elevated, while capillary density is increased. These studies suggest that angiogenesis is effected by the stimulus evoking cardiac enlargement and that a variety of factors may influence the growth of precapillary and capillary coronary vessels.

Animals↗
PubMed1987

Left ventricular hypertrophy and risk of cardiac failure: insights from the Framingham Study.

The incidence of congestive heart failure (CHF), derived from more than 30 years of follow-up, is examined by electrocardiogram (ECG) and radiography in relation to cardiac hypertrophy. Cardiac failure occurred in 485 of 5,209 subjects participating in the Framingham Study. Hypertension was the dominant predisposing factor for both cardiac hypertrophy and cardiac failure. The ECG pattern of left ventricular hypertrophy (ECG-LVH) heralded serious cardiovascular disease of all varieties, but risk ratios were two- to fivefold greater for the development of CHF in men and women (ages 35-64 years) than for any other sequelae. Risk of CHF in those with ECG-LVH exceeded that for unrecognized ECG patterns at myocardial infarction (ECG-MI). The ECG pattern of left ventricular hypertrophy, characterized by increased voltage unaccompanied by a repolarization abnormality, carried a decreased risk, chiefly reflecting the severity of coexistent hypertension. The independent contribution of ECG-LVH with accompanying repolarization changes to the risk of CHF was equal in the two sexes and persisted with advancing age. The ECG pattern of left ventricular hypertrophy was more strongly associated with occurrence of CHF than was radiographic enlargement, and contributed to the risk of CHF (taking radiographic heart size into account). Echocardiographic evidence of LVH (ECHO-LVH) was more common in subjects with CHF than was ECG-LVH, occurring in 63% of women and 77% of men with CHF, and LVH was the most frequently observed echocardiographic finding. Cardiac hypertrophy was found to be an ominous harbinger of cardiac failure, particularly when it was manifested on an ECG with repolarization abnormality.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Morphologic criteria of progression and regression of cardiac hypertrophy.

The heart is able to adapt itself to a demanded load by increasing (hypertrophy) or decreasing (regression of hypertrophy) its muscular mass within a wide range. Overstressing of the ability of adaptation is accompanied by degenerative changes of myocytes. Semiquantitative investigations of endomyocardial biopsies (EMCBs) of patients with dilative cardiomyopathy (DCM) and hypertrophic nonobstructive cardiomyopathy (HNCM) show a fibrosis of the interstitial space, as well as almost similar changes of myofibrils and mitochondria. A reduced number of myocytes in hearts with DCM could explain the decreased functional capacity. Quantitative investigations of endomyocardial biopsies and myectomy specimens in patients with hypertrophic obstructive cardiomyopathy have revealed that hypertrophy and, to a certain extent, hyperplasia of muscle fibers cause asymmetrical thickening of the septum. Experimental investigations of the regression of training-induced hypertrophy in rats have shown that nearly all parameters (cardiac weight, thickness of muscle fibers, myofibrillar mass, interstitial space, and capillary width) returned to the values of controls 14 days after termination of a swimming training regimen. A significantly higher density of capillaries after regression of muscle fiber hypertrophy compared to controls points to a temporal dissociation in the regression of myocyte size and capillary network. Decrease in RNA concentration and an increased number of autophagic vacuoles give evidence for decreased anabolism and increased catabolism may occur during regression. In humans, fibrosis of the myocardium and scar formation explain the irreversibility of cardiac hypertrophy, as observed in some patients with valvular heart disease, despite valve replacement.

Adult↗
PubMed1989

Relationship between coronary artery size and ventricular hypertrophy.

The relationship between coronary blood flow and ventricular hypertrophy has been studied in animal models. But, this relationship in the human body is scarcely evaluated. In this study we measured coronary arterial sizes by coronary arteriograms and correlated them with ventricular hypertrophy. Patients who underwent cardiac catheterization and coronary arteriography and showed no significant coronary arterial lesions were included in this study. There were 131 patients, 75 men and 56 women, with a mean age of 53 +/- 10 years (S.D.). After evaluation with electrocardiograms, echocardiograms and left ventriculograms these patients were divided into 4 groups: (1) the non-hypertrophy (NVH) group, 50 cases; (2) the left ventricular hypertrophy (LVH) group, 38 cases; (3) the right ventricular hypertrophy (RVH) group, 23 cases; and (4) the biventricular hypertrophy (BVH) group, 20 cases. The proximal portion of the 3 major coronary arteries and the left main stem were measured from coronary arteriograms with the catheter tip as a size reference. The results showed that the left main stem was larger than the 3 major coronary arteries in the NVH, LVH and BVH groups. But in the RVH group, the left main stem was not significantly larger than the right coronary artery. In all 4 groups the left circumflex coronary artery was the smallest while the left anterior descending coronary artery and the right coronary artery were similar in size. Patients with LVH showed dilatation of all 3 left coronary measurements (left main stem, left anterior descending coronary artery and left circumflex coronary artery) as compared with the NVH patients and the RVH patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Myocardial fibrosis in nonhuman primate with pressure overload hypertrophy.

Characteristics of pressure overload hypertrophy are known to include an accumulation of collagen (or fibrosis) and a biochemical remodeling of fibrillar type I and III collagens. The corresponding structural nature of myocardial fibrosis is less clear. This light morphologic study was undertaken to address this issue in the hypertrophied left ventricle of the nonhuman primate with experimental hypertension. For this purpose, the picrosirius red technique and polarization microscopy were used to examine the myocardium during the evolutionary, early, and late phases of established hypertrophy corresponding to 4, 35, and 88 weeks of experimental hypertension. Evidence of increased thin perimysial fiber formation, together with collagen fiber disruption and edema at 4 weeks of hypertrophy, was found when the chamber volume to left ventricular mass ratio was reduced. After 35 weeks, when this ratio was again normal, a greater number of intermuscular spaces contained both thick and thin perimysial fibers. In addition to this interstitial fibrosis, a reactive fibrosis consisting of a meshwork of thick and thin perimysial fibers was seen extending over muscle fibers. Finally, at 88 weeks, this fibrous meshwork had encircled muscle and there now was evidence of cell necrosis. The accompanying replacement fibrosis consisted of yet another distinctive orthogonal grid of thick and thin collagen fibers. Thus, a continuum of fibrillar collagen remodeling was seen in pressure overload hypertrophy in the nonhuman primate myocardium. Structurally distinct patterns of myocardial fibrosis were recognized based on the alignment of perimysial fibers with muscle that may explain the cellular remodeling and altered mechanical behavior of the concentrically hypertrophied myocardium.

Animals↗
PubMed1985

The influence of sympathetic nervous activity on regression of cardiac hypertrophy.

Pharmacotherapeutical means of reversing cardiac hypertrophy (prazosin, clonidine and nifedipine) were analysed in concentrically, as well as eccentrically, hypertrophied left ventricles. Regression of cardiac hypertrophy, i.e. a therapeutic intervention on a critical precursor of hypertensive congestive heart failure, can be obtained by various antihypertensive agents. Prazosin, calcium channel blockers, clonidine 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 ischaemic 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.

Animals↗