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PubMed1994

Angiotensin II maintains, but does not mediate, isoproterenol-induced cardiac hypertrophy in rats.

The role of angiotensin II (ANG II) in the development of isoproterenol (Iso)-induced cardiac hypertrophy was examined in rats. Iso increased cardiac mass, left ventricular RNA-to-DNA ratio, and the cardiac content of both myosin heavy chain and hydroxyproline in a dose-dependent manner, indicating that Iso-induced cardiac hypertrophy involves growth of both muscle and connective tissue. Cardiac hypertrophy reverted within 11-14 days after cessation of Iso. Propranolol prevented development of Iso-induced cardiac hypertrophy but did not affect the rate of its reversal. The ANG II receptor blocker losartan (Los) did not significantly decrease the hypertrophic response to Iso. Los injected after cessation of Iso dramatically enhanced the reversal of cardiac hypertrophy, even in rats that received Los with Iso during the induction of Iso-induced cardiac hypertrophy. ANG II, injected continuously at a subpressor dose that did not affect heart weight when given alone, inhibited reversal of cardiac hypertrophy when given after cessation of Iso. Los did not significantly affect the induction of the protooncogene c-fos by Iso. We conclude that endogenous ANG II has a major function in maintaining Iso-induced cardiac hypertrophy but does not mediate its induction. This suggests that different interactive stimuli may be required for development of cardiac hypertrophy, i.e., for initiation and for maintenance.

Actins↗
PubMed1996

Transient outward current in catecholamine-induced cardiac hypertrophy in the rat.

We have demonstrated that a daily injection of isoproterenol (5 mg/kg ip) for 7 days induces a 30% increment in heart weight-to-body weight ratio and prolongs the action potential duration (APD) in male Wistar rats. The underlying mechanism of the prolonged APD was investigated in this model of hypertrophy by measuring the transient outward potassium current (Ito) in left ventricular myocytes of the rat with whole cell voltage-clamp techniques. Cell membrane capacitance was increased by 39%: 122 +/- 3 (n = 23) and 171 +/- 5 (SE) pF (n = 20) in control and hypertrophy, respectively (P < 0.001). Ito was evoked in sodium-free solutions containing 0.5 mM Ca2+ and 2 mM Co2+ by step depolarizations from a holding potential of -80 mV. The amplitude of the 4-aminopyridine-sensitive Ito (at 70 mV) was reduced by 28% in hypertrophy: 3.2 +/- 0.3 (n = 23) and 2.3 +/- 0.4 (SE) nA (n = 20) in control and hypertrophy, respectively (P < 0.05). When normalized for cell capacitance, the reduction was much larger: 26.4 +/- 2.5 and 13.1 +/- 1.8 pA/pF in control and hypertrophy, respectively (P < 0.001). The voltage dependence of Ito was similar in both cell types. No change was observed in the steady-state activation and inactivation kinetics in the two groups, nor was there a change in the time dependence of inactivation. The recovery from inactivation of Ito when fitted with a monoexponential function was not changed significantly in hypertrophy: time constants = 8.2 +/- 0.4 (n = 13) and 8.3 +/- 0.3 ms (n = 12) in control and hypertrophy, respectively. These results show that Ito density is decreased in catecholamine-induced cardiac hypertrophy, but current kinetics are not affected. The reduced Ito density may underlie the prolongation of APD in this model of hypertrophy.

4-Aminopyridine↗
PubMed1993

Electrocardiographic findings of left, right and septal hypertrophy in athletic students and sedentary controls.

We have previously demonstrated increased voltage of septal, right and left ventricular depolarization in 1,299 athletic students compared to 151 sedentary controls. In the present investigation we have studied the prevalence of hypertrophy and the correlation between hypertrophy and other ECG findings. An increase of Q waves of more than 0.2 mV was associated with increased indices of right and left ventricular hypertrophy. Right ventricular hypertrophy was associated with an increased prevalence of incomplete right bundle branch block and increased parameters of septal and left ventricular hypertrophy. Left ventricular hypertrophy was associated with increased indices of septal and right ventricular hypertrophy and with bradycardia. Furthermore, left ventricular hypertrophy was characterized by ST elevation and increased T wave amplitudes, but not by repolarization abnormalities. Thus, our data point to a harmonious hypertrophy. Based on our findings we suggest the following normal limits in young people (20-30 years) according to the 97.5 percentile regarding the Sokolow index: for athletic students 5.3 (males) and 3.6 mV (females), for sedentary controls 4.0 (males) and 3.6 mV (females). It remains to be clarified whether these values are also valid in top athletes.

Adult↗
PubMed1998

Decompensation of pressure-overload hypertrophy in G alpha q-overexpressing mice.

BACKGROUND: Receptor-mediated activation of myocardial Gq signaling is postulated as a biochemical mechanism transducing pressure-overload hypertrophy. The specific effects of Gq activation on the functional and morphological adaptations to pressure overload are not known. METHODS AND RESULTS: To determine the effects of intrinsic myocyte G alpha q signaling on the left ventricular hypertrophic response to experimental pressure overload, transgenic mice overexpressing G alpha q specifically in the heart (G alpha q-25) and nontransgenic siblings underwent microsurgical creation of transverse aortic coarctation and the morphometric, functional, and molecular characteristics of these pressure-overloaded hearts were compared at increasing times after surgery. Before aortic banding, isolated G alpha q-25 ventricular myocytes exhibited contractile depression (depressed +dl/dt and -dl/dt) and G alpha q-25 hearts showed a pattern of fetal gene expression similar to the known characteristics of nontransgenic pressure-overloaded mice. Three weeks after transverse aortic banding, G alpha q-25 left ventricles hypertrophied to a similar extent (approximately 30% increase) as nontransgenic mice. However, whereas nontransgenic mice exhibited concentric left ventricular remodeling with maintained ejection performance (compensated hypertrophy), G alpha q-25 left ventricles developed eccentric hypertrophy and ejection performance deteriorated, ultimately resulting in left heart failure (decompensated hypertrophy). The signature hypertrophy-associated progress of fetal cardiac gene expression observed at baseline in G alpha q-25 developed after aortic banding of nontransgenic mice but did not significantly change in aortic-banded G alpha q-25 mice. CONCLUSIONS: Intrinsic cardiac myocyte G alpha q activation stimulates fetal gene expression and depresses cardiac myocyte contractility. Superimposition of the hemodynamic stress of pressure overload on G alpha q overexpression stimulates a maladaptive form of eccentric hypertrophy that leads to rapid functional decompensation. Therefore G alpha q-stimulated cardiac hypertrophy is functionally deleterious and compromises the ability of the heart to adapt to increased mechanical load. This finding supports a reevaluation of accepted concepts regarding the mechanisms for compensation and decompensation in pressure-overload hypertrophy.

Animals↗
PubMed1987

Influence of blood pressure on development of aortic medial smooth muscle hypertrophy in spontaneously hypertensive rats.

The hypothesis that a primary stimulus for aortic medial hypertrophy in spontaneously hypertensive rats (SHR) is increased blood pressure was tested by determining whether development of smooth muscle cell hypertrophy and hyperploidy in SHR could be dissociated from blood pressure levels in rats treated with various antihypertensive drugs with different mechanisms of action. Wistar-Kyoto rats (WKY) and SHR were treated between 2 and 5 months of age with captopril (375 mg/L), hydralazine (40 mg/L), or propranolol (1.5 mg/L) administered in their drinking water. Smooth muscle hypertrophy and hyperploidy were analyzed by morphometric evaluation of medial smooth muscle content, flow cytometric analysis of the frequency of polyploid smooth muscle cells, and biochemical estimates of smooth muscle cell number. All drugs significantly lowered blood pressure in SHR compared with untreated controls (order of efficacy: captopril greater than hydralazine greater than propranolol). Captopril also was most effective at changing blood pressure in WKY, while propranolol and hydralazine had similar blood pressure-lowering effects. The efficacy of drugs in preventing the development of smooth muscle cell polyploidism and medial hypertrophy in SHR was the same as their efficacy in lowering blood pressure, although propranolol had no effect on medial smooth muscle hypertrophy despite lowering blood pressure by 26 mm Hg. Regression analyses showed a high degree of correlation between blood pressure and the frequency of polyploid smooth muscle cells and medial smooth muscle content. These results are consistent with the hypothesis that aortic medial hypertrophy may be, in part, a response to increased blood pressure or wall stress. However, analysis of covariance and two-stage multiple regression analyses indicated that captopril had an effect over and above that predicted by its blood pressure-lowering effect. Furthermore, propranolol lowered blood pressure but did not affect medial hypertrophy. These results suggest that smooth muscle hypertrophy is not simply a response to increased blood pressure, but that other factors, such as angiotensin II, may be important in modulating aortic medial hypertrophy in SHR.

Animals↗
PubMed1988

Diminished cardiac hypertrophy and muscle performance in older compared with younger adult rats with chronic atrioventricular block.

The combined effect of advancing age and hemodynamic overload on cardiac muscle function has received little attention. In male, Sprague-Dawley rats, we studied the interaction of chronic atrioventricular heart block induced by transvenous electrocautery for 4-12 months (mean, 7 months) and age at study (12, 19 +/- 0.7, and 24 +/- 0.2 months) on cardiac hypertrophy and muscle function compared with age-matched, sham-operated controls. Hypertrophy was determined by the ratio of heart weight to tibial length. Muscle function was first determined from the mechanical variables of the isometric contraction of an excised, thin, left ventricular trabecular muscle bathed at 29 degrees C under a variety of calcium concentrations and stimulation patterns. Then, in the same muscles after disruption of membranes with Triton X-100, the force-pCa curve of the myofibrils was obtained. No hypertrophy occurred with aging in the control group, but alteration in hypertrophy with age occurred in the block group such that the youngest animals with block had the most hypertrophy (170%) and the oldest animals with block the least hypertrophy (120%). The tension developed by cardiac muscle and the duration of the isometric contraction were not affected by age in the control group but were significantly affected by age in the block group. The young animals with block had a markedly prolonged contraction duration and almost twice the developed tension compared with the older animals with block or with controls. The age-related difference in muscle contraction duration in the block group was associated with, and may have only been secondary to, the age-related difference in the extent of cardiac hypertrophy. For developed tension, the age-related difference in the block group could not be explained by differences in the extent of cardiac hypertrophy. Rather, this difference was attributable to both an increased myofibrillar force-generating capacity in the young block and to an impairment in excitation-contraction coupling in the old block. The results show that during long-term block, age exerted not only a significant effect on the extent of cardiac hypertrophy but also an independent effect on the developed tension of cardiac muscle.

Aging↗
PubMed1990

Functional and morphological characteristics of compensated and decompensated cardiac hypertrophy in dogs with chronic infrarenal aorto-caval fistulas.

The relation between cardiac hypertrophy, shunt size, myocardial contractility, capillary density, adrenergic responsiveness, and neurohumoral stimulation was evaluated in dogs with compensated and decompensated cardiac hypertrophy caused by an infrarenal aorto-caval shunt. Shunt size varied from 5 to 35 mm2 due to an inability to create a uniform size. Dogs that developed heart failure within 4 months had 25 +/- 2 mm2 shunts, whereas those that developed it after 4 months had 19 +/- 3 mm2 shunts; those that did not develop heart failure had 10 +/- 1 mm2 shunts. Hypertrophy developed at the same rate in all the dogs that developed heart failure, which occurred at a critical heart weight (hypertrophy) for a given load (shunt size). In the dogs with heart failure there was a decrease in myocardial contractility (tension = 5.7 +/- 0.6 vs. 7.3 +/- 0.3 g/mm2, p less than 0.05), a decrease in adrenergic responsiveness (maximal heart rate with isoproterenol = 203 +/- 7 vs. 249 +/- 5 beats/min, p less than 0.01), an increase in circulating neurohormones, and a decrease in urinary sodium excretion (0.4 +/- 0.1 vs. 5.0 +/- 1.3 meq/3 hr, p less than 0.01). None of these abnormalities occurred in dogs with compensated hypertrophy. There were no differences in cardiac capillary density between the control dogs and the dogs with compensated cardiac hypertrophy or heart failure. Thus, it would appear that if heart failure is to develop after an initial toleration of a sudden volume overload, it will develop at a given combination of cardiac hypertrophy and volume overload, with cardiac hypertrophy developing at the same rate in all cases. In this model, once heart failure develops, myocardial contractility and cardiac adrenergic responsiveness are decreased and there is pronounced neurohumoral activation. All these changes are absent in hearts with compensated hypertrophy.

Adaptation, Physiological↗
PubMed1991

Cellular versus myocardial basis for the contractile dysfunction of hypertrophied myocardium.

Contractile dysfunction has been demonstrated in many previous studies of experimental right ventricular pressure-overload hypertrophy; however, given the complex changes that occur both in the cardiac muscle cell and in the multiple components of the cardiac interstitium, it is not clear whether the contractile dysfunction observed is an intrinsic property of the cardiac muscle cell or whether it is the result of a mechanically normal cardiac muscle cell contracting within an abnormal interstitial environment. The purpose of the present study was to examine the contractile behavior of cardiac muscle cells, or cardiocytes, isolated from seven cat right ventricles that were pressure-overloaded by banding the pulmonary artery; right ventricular cardiocytes from seven sham-operated cats served as controls. Cardiocytes were obtained from these cats via standard cell isolation procedures; contractile function of the cardiocytes in response to graded viscous external loads was defined by laser diffraction. The cells were stimulated to contract at a frequency of 0.25 Hz, using 100-microA direct current pulses of alternating polarity. Hypertrophied right ventricular cardiocytes obtained from banded cats showed marked systolic contractile abnormalities in comparison with right ventricular cardiocytes from sham-operated cats. The peak velocity of sarcomere shortening for the control and hypertrophied cardiocytes in 1-cp superfusate was 3.6 +/- 0.2 and 2.1 +/- 0.1 microns/sec, respectively (p less than 0.001); the maximum extent of sarcomere shortening for the control and hypertrophied cardiocytes was 0.21 +/- 0.01 and 0.14 +/- 0.01 microns, respectively (p less than 0.001). Further, the time to peak shortening in the 1-cp superfusate was significantly longer for the hypertrophied cardiocytes (150.1 +/- 3.3 versus 160.4 +/- 3.7 msec; p less than 0.04). When the relengthening properties of the cells were examined in the 1-cp superfusate, there were significant differences between cardiocyte groups. The peak rate of sarcomere relengthening was 3.5 +/- 0.2 microns/sec in the control cardiocytes and 2.2 +/- 0.17 microns/sec in the hypertrophied cardiocytes (p less than 0.001). Similarly, the time to peak velocity of sarcomere relengthening (48.8 +/- 1.8 versus 57.9 +/- 2.9 msec) and the time to 50% maximal sarcomere relengthening (57.1 +/- 3.1 versus 67.1 +/- 3.1 msec) were both significantly prolonged for the hypertrophied cardiocytes (p less than 0.02). This study shows for the first time that the contractile defect in this model of right ventricular pressure-overload hypertrophy is intrinsic to the cardiac muscle cell itself. This finding provides a basis for further, more focused investigations designed to determine the mechanisms responsible for the contractile dysfunction observed in this form of experimental cardiac hypertrophy.

Animals↗
PubMed1998

Cytoskeletal role in the transition from compensated to decompensated hypertrophy during adult canine left ventricular pressure overloading.

Increased microtubule density causes cardiocyte contractile dysfunction in right ventricular (RV) pressure-overload hypertrophy, and these linked phenotypic and contractile abnormalities persist and progress during the transition to failure. Although more severe in cells from failing than hypertrophied RVs, the mechanical defects are normalized in each case by microtubule depolymerization. To define the role of increased microtubule density in left ventricular (LV) pressure-overload hypertrophy and failure, in a given LV we examined ventricular mechanics, sarcomere mechanics, and free tubulin and microtubule levels in control dogs and in dogs with aortic stenosis both with LV hypertrophy alone and with initially compensated hypertrophy that had progressed to LV muscle failure. In comparing initial values with those at study 8 weeks later, dogs with hypertrophy alone had a very substantial increase in LV mass but preservation of a normal ejection fraction and mean systolic wall stress. Dogs with hypertrophy and associated failure had a substantial but lesser increase in LV mass and a reduction in ejection fraction, as well as a marked increase in mean systolic wall stress. Cardiocyte contractile function was equivalent, and unaffected by microtubule depolymerization, in cells from control LVs and those with compensated hypertrophy. In contrast, cardiocyte contractile function in cells from failing LVs was quite depressed but was normalized by microtubule depolymerization. Microtubules were increased only in failing LVs. These contractile and cytoskeletal changes, when assayed longitudinally in a given dog by biopsy, appeared in failing ventricles only when wall stress began to increase and function began to decrease. Thus, the microtubule-based cardiocyte contractile dysfunction characteristic of pressure-hypertrophied myocardium, originally described in the RV, obtains equally in the LV but is shown here to have a specific association with increased wall stress.

Analysis of Variance↗
PubMed2002

Mibefradil improves beta-adrenergic responsiveness and intracellular Ca(2+) handling in hypertrophied rat myocardium.

The present study investigated the effects of mibefradil, a novel T-type channel blocker, on ventricular function and intracellular Ca(2+) handling in normal and hypertrophied rat myocardium. Ca(2+) transient was measured with the bioluminescent protein, aequorin. Mibefradil (2 microM) produced nonsignificant changes in isometric contraction and peak systolic intracellular Ca(2+) concentration ([Ca(2+)](i)) in normal rat myocardium. Hypertrophied papillary muscles isolated from aortic-banded rats 10 weeks after operation demonstrated a prolonged duration of isometric contraction, as well as decreased amplitudes of developed tension and peak Ca(2+) transient compared with the sham-operated group. Additionally, diastolic [Ca(2+)](i) increased in hypertrophied rat myocardium. The positive inotropic effect of isoproterenol stimulation was blunted in hypertrophied muscles despite a large increase in Ca(2+) transient amplitude. Afterglimmers and corresponding aftercontractions were provoked with isoproterenol (10(-5) and 10(-4) M) stimulation in 4 out of 16 hypertrophied muscles, but were eliminated in the presence of mibefradil (2 microM). In addition, hypertrophied muscles in the presence of mibefradil had a significant improvement of contractile response to isoproterenol stimulation and a reduced diastolic [Ca(2+)](I), although a mild decrease of peak Ca(2+)-transient was also shown. However, verapamil (2 microM) did not restore the inotropic and Ca(2+) modulating effects of isoproterenol in hypertrophied myocardium. Mibefradil partly restores the positive inotropic response to beta-adrenergic stimulation in hypertrophied myocardium from aortic-banded rats, an effect that might be useful in hypertrophied myocardium with impaired [Ca(2+)](i) homeostasis.

Adrenergic beta-Agonists↗
PubMed2002

Inhibitory molecules in signal transduction pathways of cardiac hypertrophy.

Cardiac hypertrophy is induced by a variety of diseases, such as hypertension, valvular diseases, myocardial infarction, and endocrine disorders. Although cardiac hypertrophy may initially be a beneficial response that normalizes wall stress and maintains normal cardiac function, prolonged hypertrophy is a leading cause of heart failure and sudden death. A number of studies have elucidated molecules responsible for the development of cardiac hypertrophy, including the mitogen-activated protein (MAP) kinases pathway, Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, and calcium/calmodulin-dependent protein phosphatase calcineurin pathway. These molecules may be targets for therapies designed to prevent the progression of cardiac hypertrophy. Numerous studies have focused on characterization of the intracellular signal transduction molecules that promote cardiac hypertrophy in order to clarify the molecular mechanisms, but there have been only a few reports on the inhibitory regulators of hypertrophic response. Recently, several molecules have attracted much attention as endogenous inhibitory regulators of cardiac hypertrophy. Enhancement of these inhibitory regulators would also seem to be a potential approach for the pharmacological treatment of hypertrophy. In this review, we summarize the inhibitory molecules of cardiac hypertrophy.

Animals↗
PubMed1976

Giant T wave inversion as a manifestation of asymmetrical apical hypertrophy (AAH) of the left ventricle. Echocardiographic and ultrasono-cardiotomographic study.

Left ventricular scanning by echocardiography and ultrasono-cardiotomography was performed to search the possible muscular abnormality in 9 cases with giant T wave inversion without documented cause. The deeply inverted T wave was more than 1.2 mV (average was 1.63 mV) in the left precordial leads. All the cases had electrocardiographic left ventricular hypertrophy of obscure origin and ischemic episode was absent. Conventional echo beam direction to measure the short axis of the left ventricle disclosed almost normal thickness and movement of both interventricular septum (IVS) and the posterior wasll (PW), so that the report of these cases is frequently within normal limits. However, ultrasono-cardiotomography (sector B scan) disclosed the fairly localized hypertrophy near the left ventricular apex, and conventional echocardiography also revealed the same area of either IVS or PW or both below the insertion of the papillary muscles, when the scanning towards the apex was performed (asymmetrical apical hypertrophy: AAH). Control study of 9 cases with IHSS showed asymmetrical septal hypertrophy (ASH) with almost equally hypertrophied IVS from base to apex. All cases had inverted T waves, but these were of lesser degree. Three cases had relatively deep T wave compatible with those of AAH, and these cases also had the apical hypertrophy of considerable degree (unusual type of IHSS, i.e., intermediate type between AAH and ASH). The close relationship between the depth of the inverted T waves and the Apex/Mid wall thickness ratios suggests that the altered recovery process of the hypertrophied apical musculature is responsible for the giant T wave inversion of heretofore unsolved origin. Until the connective link of AAH to the other forms of hypertrophic cardiomyopathy is disclosed, the cases with such a T wave and the apical hypertrophy may be designated as asymmetrical apical hypertrophy (AAH).

Adult↗
PubMed1986

Left ventricular hypertrophy. A cardiovascular risk factor in essential hypertension.

The heart adapts to increasing afterload, such as that which occurs in arterial hypertension, with an increase in wall thickness in order to bring wall stress back to normal. As a consequence, concentric left ventricular hypertrophy ensues. Hypertension as well as advancing age has been shown to be associated with an increase in posterior wall thickness. Accordingly, the prevalence of left ventricular hypertrophy becomes very high in the elderly and may occur in more than 50% of elderly hypertensive patients. Left ventricular hypertrophy is not merely a physiological process serving to compensate for the increased afterload. The Framingham study has indicated that patients with left ventricular hypertrophy are at an increased risk of sudden death and other cardiovascular morbidity and mortality. The risk for sudden death is 5 to 6 times higher in patients with left ventricular hypertrophy than in those without, regardless of levels of arterial pressure. By Holter monitoring of these patients it has been shown that those with left ventricular hypertrophy have a prevalence of premature ventricular contractions that is 40 to 50 times higher than those patients without left ventricular hypertrophy. In addition, patients with left ventricular hypertrophy rated substantially higher with regard to Lown's classes than those without. These data indicate that left ventricular hypertrophy is common, particularly in the elderly, and predisposes to ventricular ectopy, higher grade arrhythmias, and sudden death. Clearly, these considerations have to be taken into account when selecting antihypertensive therapy inasmuch as hypokalaemia, hypomagnesaemia, and other electrolyte shifts predisposing to ventricular arrhythmias must be scrupulously avoided.

Age Factors↗
PubMed1990

Reversal of left ventricular hypertrophy: a desirable therapeutic goal?

It is controversial whether myocardial hypertrophy in essential hypertension represents an adaptive physiologic or pathological response to increased pressure load imposed on the heart. Cardiac structural adaptations in endurance athletes fulfill the criteria of physiologic hypertrophy: maintained cardiac performance and full reversibility of cardiac structural changes following cessation of endurance training. In contrast, there is some evidence that cardiac hypertrophy in arterial hypertension is a pathological process. Diastolic function of the left ventricle is impaired; systolic function, although maintained in the early stages of myocardial hypertrophy, becomes reduced beyond a critical mass; and cardiac structural changes are not fully reversible. An increasing number of prospective studies document that left ventricular hypertrophy in essential hypertension represents an independent risk factor for cardiovascular mortality and morbidity, in particular for sudden cardiac death. Ventricular arrhythmias were regarded as the pathophysiologic link between cardiac structural adaptation and the increased risk of sudden death due to left ventricular hypertrophy. Structural changes of the coronary circulation may represent one confounding factor in the relationship between left ventricular hypertrophy and its cardiovascular risk. As a consequence, optimal antihypertensive therapy should aim at reducing both arterial hypertension and left ventricular hypertrophy. Whether regression of myocardial hypertrophy indeed reduces cardiovascular risk cannot be definitively answered from the available data.

Cardiomegaly↗
PubMed1986

Sarcomere shortening in pressure overload hypertrophy.

Sarcomere shortening during contraction was measured by using laser diffraction, in thin, rabbit right ventricular (RV) trabeculae from normal hearts (N) (n = 5) and from hearts subjected to RV pressure overload by pulmonary banding (H) (n = 5). Banding resulted in substantial RV hypertrophy after 2 wk. Hypertrophied preparations had the same resting muscle length (H = 3.15 +/- 0.29 mm) and resting sarcomere lengths (H = 2.16 +/- 0.005 micron) as the normal preparations (3.10 +/- 0.37 mm, 2.16 +/- 0.008 micron, respectively). Total tension at the peak of isometric twitches was the same as normal in the hypertrophied muscles (N = 8.06 +/- 1.20, H = 8.51 +/- 1.95 g/mm2). However, the amount of auxotonic sarcomere shortening was much less than normal in the hypertrophied preparations (N = 0.39 +/- 0.028, H = 0.19 +/- 0.034 micron; P less than 0.001). In isotonic contractions in which the ratio of muscle shortening to resting muscle length was the same in both the normal and hypertrophied muscles (ratio of 0.05 in both groups), the extent of sarcomere shortening relative to resting sarcomere length was less in the hypertrophied muscles than in the normal preparations (N = 0.14 +/- 0.01), H = 0.07 +/- 0.01; P less than 0.01). Series elasticity was the same as normal in the hypertrophied muscle P less than 0.05). Less auxotonic sarcomere shortening for a given level of isometric tension development and less isotonic sarcomere shortening per unit muscle shortening indicate that there is less than normal work per sarcomere during contraction in hypertrophied myocardium. These findings may have important implications for intracellular compensatory adaptation in pressure overload cardiac hypertrophy.

Animals↗
PubMed1978

[The heart in hypertension. V. Systolic and diastolic wall stress and degree of hypertrophy as determinants of diagnostic and therapeutical consequences (author's transl)].

The appropriateness of hypertrophy was analyzed in 64 patients with essential hypertension during diagnostic cardiac catheterization and left ventriculography. The degree of hypertrophy may be described by the relationships between peak systolic pressure, mass to volume ratio and peak systolic wall stress. The peak systolic wall stress represents an important determinant of the appropriateness of hypertrophy and has great influence on left ventricular function and myocardial energy demand. The hypertrophy in essential hypertension may be subdivided into 3 different types of hypertrophy: (a) inappropriate hypertrophy associated with increased mass-to-volume ratio and decreased systolic wall stress, (b) appropriate hypertrophy with normal systolic wall stress and (c) inappropriate hypertrophy with normal or decreased mass-to-volume ratio, however with significantly increased systolic wall stress. On the basis of the appropriateness or degree of left ventricular hypertrophy in essential hypertension the therapeutical consequences are being discussed with special reference to beta receptor blockade and digitalis glycosides.

Adrenergic beta-Antagonists↗
PubMed1981

[Secondary atypical hypertrophy: hypertrophic cardiomyopathy with acquired risk factors (author's transl)].

New clinical concept of "secondary atypical hypertrophy" was proposed for hypertrophic cardiomyopathy (HCM) associated with an acquired risk factors such as hypertension, strenuous exercise, etc, based on the following findings. 1) Case-control study suggested that history of hypertension, physical labor and weight gain were thought to be risk factors of apical hypertrophy. History of hypertension was also demonstrated in 55% of older cases of HCM (greater than 35 yrs) with asymmetric septal hypertrophy, and this figure was appreciably higher than that in general population (around 26% in our population survey). Thus hypertension was suggested to have a causal relationship to HCM as an important risk factor in older cases. 2) Even in cases without hypertension, 29% of non-obstructive HCM exhibited a marked increase in systolic blood pressure on bicycle ergometer stress test, suggesting an important of transient hypertension during exercise as a risk factor of unusual hypertrophy. 3) The cases of HCM with definite family history and the cases of HCM with secondary atypical hypertrophy, with acquired risk factors such as hypertension, presented different clinical features. The latter is older and predominant in males. In the former, QRS pattern was les distorted, suggesting milder congenital defect of the myocardium. Left ventricular function was less impaired in cases with secondary atypical hypertrophy if judged from diastolic descent rate of the mitral valve, left ventricular enddiastolic pressure and functional aerobic impairment (FAI). On the other hand, no differences were observed between cases with ventricular septal hypertrophy and left ventricular outflow obstruction. 4) Follow-up study demonstrated rather favorable prognosis in cases with secondary atypical hypertrophy because of the absence of sudden death despite of their older age. These distinctive difference in clinical features, prognosis and then management in cases with HCM with acquired risk factors suggested a validity of the concept of secondary atypical hypertrophy in clinical practice.

Adult↗
PubMed1995

The effects of compensated cardiac hypertrophy on dihydropyridine and ryanodine receptors in rat, ferret and guinea-pig hearts.

The number of dihydropyridine and ryanodine receptors (DHP-R and RyR) has been measured in control and hypertrophied ventricles from rats, guinea pigs and ferrets to determine whether these two channels contribute to the alterations in excitation-contraction coupling (ECC), and in Ca2+ transient during compensated cardiac hypertrophy. We found that ventricular hypertrophy did not change the density of DHP-R. Mild hypertrophy did not alter the density of RyR in the rat but decreased it in the guinea-pig and in the ferret (30% and 36%, respectively). Severe hypertrophy decreased the density of RyR by 20% in the rat and by 34% in the guinea-pig. Therefore, the decrease is greater in ferret and guinea-pig hearts than in rat heart. We conclude that the sarcoplasmic reticulum (SR) Ca2+ release channels but not the L-type Ca2+ channels could contribute to the slowing of intracellular Ca2+ movements and to the reduced velocity of shortening of the hypertrophied hearts. We suggest that, in the guinea pig and ferret hearts which express only the beta myosin heavy chain (MHC) isoform, the reduced velocity of shortening during hypertrophy is related to the decrease in RyR density, whereas in the rat, it is regulated primarily via a shift in the MHC isoform, except in severe hypertrophy in which the moderate decrease in RyR would also be involved.

Adaptation, Physiological↗