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PubMed2000

[Effects of amiloride on calcium current in thyroxine-induced hypertrophied rat heart].

AIM: The L-Type calcium currents were investigated in normal, hypertrophied and amiloride-treated rat ventricular myocytes so as to clarify the possible cause of the action potential lengthening that has been reported in thyroxine-induced hypertrophy. The interactions between agents such as thyroxine, Ang II and phenylephrine which induced hypertrophy with amiloride on the calcium current were analyzed. METHODS: Myocardial hypertrophy was induced by i.p. L-thyroxine in rats. The cell length, cell width and cell area were measured by image analysis technique. For recording ICaL, the whole cell patch clamp technique was used. Potassium currents were suppressed by replacing K+ ions with Cs+ ions in intracellular media, and sodium current was blocked by 50 mumol.L-1 tetrodotoxin. RESULTS: The Ca2+ current was found to be larger in hypertrophied cells (783pA) than in normal cells (433pA) and in amiloride-treated cells (429pA). However, no significant difference was observed in current density (6.54, 8.33, 5.74 pA/pF) in normal, hypertrophied and amiloride-treated cells. ICa displayed the same voltage dependence in three cell types. The potential giving 50% of activation (V1/2) moved towards more negative and the slope of activation curve was smaller in hypertrophied cells than in normal cells and amiloride cells. When expressed as percentages, the maximal increases in ICa were obtained with 1 mumol.L-1 Ang II and 100 mumol.L-1 phenylephrine in normal cells (+45.5% and +81.8%). Thyroxine 100 mumol.L-1 showed no effect on ICa. After giving amiloride, Ang II and phenylephrine did not increase the amplitude of ICa. CONCLUSION: At the dose of 0.5 mg.kg-1.d-1, amiloride (p.o.) was shown to prevent the amplitude of ICa from increasing and to be effective against increases of amplitude of ICa by Ang II and phenylephrine.

Amiloride↗
PubMedDate not supplied

[ECG mapping in heart muscle hypertrophy].

67 test persons (15 healthy persons, 52 patients with coronary heart disease, of them 28 patients with and 24 patients without myocardial hypertrophy) were examined by means of a mapping ECG (69 leads) and the echocardiography. For every individual lead of the mapping ECG the mean values and simple scattering of the R and S potentials of 15 normal persons have been established. Of this we led the limit values for left heart and right heart hypertrophy for every individual lead. We are able to make evident that for the determination of a myocardial hypertrophy the principle of Sokolow's index can be transferred to R (max) and S (min) of the mapping ECG. A quantification of the myocardial hypertrophy by means of the R-potential summation method presupposes a correction of the normal potential decrease in the cardio-electric field. A regionally differently characterized myocardial hypertrophy can be recognized with the help of the mapping ECG. By means of an exercise-induced mapping ECG hypertrophy-caused repolarisation disturbances can highly significantly be demarcated (p less than 0.001) from ischaemia-caused ones. The difference mapping is suitable as mapping ECG documentation for a myocardial hypertrophy.

Cardiomegaly↗
PubMed1991

[ACE inhibition: mechanisms of cardioprotection in heart hypertrophy].

Epidemiologic studies have revealed that in arterial hypertension left ventricular hypertrophy is an important risk factor for cardiac failure. Accordingly antihypertensive therapy should aim at preventing or regressing left ventricular hypertrophy. Reduction of blood pressure does not necessarily induce reversal of left ventricular hypertrophy. Vasodilators like hydralazine and minoxidil, which lead to augmented plasma levels of norepinephrine, were not able to diminish left ventricular hypertrophy. In contrast, a sympatholytic therapy with methyldopa caused a reversal of left ventricular muscle mass. These experimental findings in spontaneously hypertensive rats led to the hypothesis that catecholamines control the onset and progression of myocardial hypertrophy mostly independent of blood pressure. This hypothesis was supported by the experimental findings, that subhypertensive dosages of norepinephrine induce left ventricular hypertrophy and that this hormone promotes alpha-receptor mediated growth of isolated myocytes. Recent studies have revealed that also the renin-angiotension-system has trophic effect on the myocardium. Clinical investigations have documented regression of cardiac hypertrophy due to antihypertensive therapy with sympatholytic drugs, ACE-inhibitors, calcium-channel blockers and beta-receptor blockers. Diuretics failed to decrease left ventricular muscle mass along with blood pressure normalization.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

[Hypertrophy and function of the left heart ventricle in hypertension].

Left ventricular hypertrophy in arterial hypertension occurs in over 50% of patients. The detection of such high incidence has been facilitated by the introduction of echocardiography into diagnostic studies. Both earlier electrocardiographic findings and later echocardiographic results show that cardiac hypertrophy leads to an increased mortality and predisposes to cardiac arrhythmias, ischemic heart disease including myocardial infarction and heart failure. The development of hypertrophy is mediated by hemodynamic factors such as elevated blood pressure due to increased peripheral vascular resistance, ejection fraction, increased cardiac output, blood viscosity, as well as by non-hemodynamic factors. Of the latter ones the contribution of a genetic factor is discussed, whereas the role of para- and autocrine cardiac function manifested by local production and action of catecholamines as well as the renin-angiotensin system has been proved. Blockade of these systems makes possible prevention of the development of cardiac hypertrophy or its regression. Such results have been obtained both in experimental studies and in humans with hypertension treated with selected drugs. Regression of hypertrophy is accompanied by an improvement in systolic and especially diastolic cardiac function, the impairment of which is usually diagnosed prior to the detection of hypertrophy. The improvement in cardiac function and possibility of preventing consequences of hypertrophy help us to evaluate the efficacy of hypotensive drugs and their preferential use in this regard. There are also changes in recently recommended models of pharmacological treatment in arterial hypertension.

Animals↗
PubMed1991

[The force-velocity relation and end systolic tension-length relation of hypertrophied myocardium in renal hypertensive rats].

Renovascular hypertension was induced in rats by left renal artery constriction. Force-velocity relation, end systolic tension-length relation (ESTLR) and responses to high extracellular calcium were investigated in hypertrophied myocardium with 4-week hypertension. The results showed that: (1) The myocardial hypertrophy was accompanied by increased peak active tension, decreased maximal velocity of shortening and prolonged contraction duration (P less than 0.01). (2) The ESTLR in hypertrophied myocardium was similar to that in the control, fitted well by an exponential curve and did not show significant alterations in all its regression parameters (P greater than 0.05). (3) No significant difference about the responses to high extracellular calcium (4 mmol/L) was observed between the control and the hypertrophied myocardium (P greater than 0.05). It is concluded that the mechanical properties of hypertrophied myocardium were characterized by a dissociation between force development and velocity of shortening and possibly these contractile abnormalities at the early stage of cardiac hypertrophy are not related to ability of calcium transport in cardiac plasma membrane. The indexes of myocardial mechanics are more sensitive to changes in contractility of hypertrophied myocardium as compared with the parameters of ESTLR.

Animals↗
PubMed1990

Reduced subendocardial coronary reserve. A potential mechanism for impaired diastolic function in the hypertrophied and failing heart.

The association between pressure overload, left ventricular (LV) hypertrophy and failure, and abnormalities in diastolic function has been described both clinically and experimentally. The mechanisms underlying this association, however, are complex and controversial. Factors that have been implicated include mechanical alterations due to hypertrophy alone, changes in collagen type and content, alterations in beta-adrenergic responsiveness, and chronic myocardial ischemia. Studies in our laboratory have identified limitations in subendocardial flow reserve in compensated LV hypertrophy and near exhaustion in subendocardial reserve in animals with decompensated LV hypertrophy and failure. These abnormalities in coronary reserve are associated with impaired diastolic function, particularly during periods of physiological stress. For example, with pacing-induced stress, impairment in diastolic function was observed in conscious dogs with compensated LV hypertrophy. In conscious dogs with LV hypertrophy and failure, isoproterenol also resulted in altered diastolic function. Thus, in the model of severe pressure-overload hypertrophy, which is characterized by limitations in coronary reserve, the mechanism of subendocardial ischemia might be responsible in part for the impairment in diastolic function observed in response to superimposed stress.

Animals↗
PubMed1990

[Remission of left ventricular hypertrophy of hypertensive origin. Experimental data].

Left ventricular hypertrophy is an adaptation of the cardiac fibre to the imposed mechanical overload. This adaptation is quantitative; increased numbers of contractile units with decreased wall stress. Qualitative changes in genomic expression allow the hypertrophied cardiac fibre to develop a normal active tension at the expense of its maximal shortening velocity. These changes are preceded by the temporary expression of proto-oncogenes, of genes of the proteins of thermal shock and by reorganisation of the cytoskeleton, all possible candidates of the regulation of the gene expression in cardiac hypertrophy. In the long-term, the hypertrophy becomes harmful: inadequate subendocardial vascular development; the lowering of the Vmax is beneficial at cellular level but eventually affects cardiac output; ventricular compliance decreases with the development of fibrosis; changes in calcium metabolism are arrhythmogenic. Modifying, prolonging and improving the natural process of adaptation is clearly the first therapeutic objective in order to decrease the hypertension and cause the hypertrophy to regress. Propranolol acts by reducing the cardiac work load. However, betablockers have the disadvantage of increasing the relative density of the subendocardial collagen. Rilmenidine decreases the quantity and density of the collagen. Vasodilators and diuretics induce regression of the myocytic hypertrophy by lowering the threshold of adaptation of these cells, but they have no effect on collagen synthesis. Angiotensin converting enzyme inhibitors which have been shown to be beneficial in controlling hypertension, induce a decrease in the hypertrophy of the myocytes and reduce fibrosis.

Cardiomegaly↗
PubMed1990

Left ventricular hypertrophy, arterial hypertension and sudden death.

Left ventricular hypertrophy has been identified as a powerful risk factor for sudden death and for general cardiovascular morbidity and mortality. Left ventricular hypertrophy has been documented as giving rise to ventricular ectopy, even in the absence of myocardial ischemia. Mechanisms of ectopic impulse generation in left ventricular hypertrophy are multifactorial and involve enlarged myocytes, focal areas of fibrosis, and subendocardial ischemia, as well as medial hypertrophy of the coronary arteries impeding homogeneous impulse propagation throughout the myocardium. Left ventricular hypertrophy can be reduced by specific antihypertensive therapy although not all antihypertensive agents are equally effective. A reduction of left ventricular hypertrophy with calcium antagonists, and possibly also with beta-blockers, has been shown to diminish ventricular arrhythmias. Whether or not such a reduction of left ventricular hypertrophy and suppression of ventricular ectopy will improve their unfavorable prognosis remains to be determined.

Antihypertensive Agents↗
PubMed1990

Diastolic properties of hypertrophied hearts in essential hypertension: classification by left ventricular wall stress.

Hypertensive cardiac hypertrophy of 20 patients was classified as inappropriate hypertrophy (HH-I) and appropriate hypertrophy (HH-II) according to their end-systolic wall stress, as measured by echocardiography. The differences in systolic and diastolic performances among the HH-I and HH-II subjects and 10 normal controls (NC) before and during isoproterenol infusion were investigated. Eight patients had subnormal end-systolic wall stress (inappropriate hypertrophy) and 12, normal end-systolic wall stress (appropriate hypertrophy). Before isoproterenol infusion, normalized peak rate of a change in left ventricular diameter during systole was significantly greater in HH-I (3.5 +/- 0.8/s) than in NC (2.3 +/- 0.5/s) and HH-II (2.6 +/- 0.6/s) (p less than 0.01 and p less than 0.005), but there was no significant difference between HH-II and NC. There was no significant difference in normalized peak rate of a change of left ventricular diameter during the rapid filling phase among the three groups (4.5 +/- 1.2/s in HH-I, 4.0 +/- 1.6/s in HH-II, and 4.2 +/- 0.8/s in NC). During isoproterenol infusion, normalized peak rate of a change of left ventricular diameter during systole was significantly greater in HH-I (7.0 +/- 1.9/s) than in HH-II (4.8 +/- 1.7/s) and NC (4.8 +/- 0.8/s) (p less than 0.05 and p less than 0.01, respectively), but there was no significant difference between HH-II and NC. Normalized peak rate of a change of left ventricular diameter during rapid filling was significantly less in HH-II (4.8 +/- 1.7/s) than in HH-I (7.3 +/- 1.3/s) and NC (6.5 +/- 0.8/s) (p less than 0.005 and p less than 0.005, respectively), but there was no significant difference between HH-I and NC. These results suggest that hypertensive patients with inappropriate hypertrophy have relatively diminished diastolic velocity (supernormal systolic velocity and normal diastolic velocity) before and during isoproterenol infusion, and that hypertensive patients with appropriate hypertrophy have absolutely diminished diastolic velocity during isoproterenol infusion, in spite of normal diastolic velocity before the infusion.

Adult↗
PubMed1987

Alpha-1 adrenoceptors in human prostate: characterization and alteration in benign prostatic hypertrophy.

Alpha-1 adrenoceptors in hypertrophied prostates of humans were characterized by a binding assay using [3H]prazosin as a radioligand. Specific [3H]prazosin binding in hypertrophied prostates of humans was saturable and of high affinity (Kd = 0.6 nM) with a maximal number of binding sites of 106 fmol/mg of protein, and it showed a pharmacological specificity as well as stereo-selectivity which characterized alpha-1 adrenoceptors. Adrenergic antagonists competed for the binding in order: R-(-)-YM-12617(5-[2-[[2-(o-ethoxyphenoxy)ethyl]amino]propyl]-2- methoxybenzenesulfonamide HCl) greater than (+/-)-YM-12617 = prazosin greater than phentolamine greater than S-(+)-YM-12617 greater than idazoxan. R-(-)- and (+/-)-YM-12617, alpha-1 adrenoceptor antagonists, have been shown to exhibit an extremely high affinity for prostatic [3H]prazosin binding sites (Ki = 0.6 and 1.1 nM, respectively). In addition, R-(-)-YM-12617 was approximately 100 times as potent as the S-(+)-isomer. The affinities of prazosin and YM-12617 compounds for [3H]prazosin binding sites in hypertrophied prostates of humans correlated closely with their pharmacological potencies in prostates reported previously. The blockade of [3H]prazosin binding sites in hypertrophied prostates of humans induced by (+/-)-YM-12617 was easily reversed by washing. There was a significant 35% increase in the maximal number of binding sites for [3H] prazosin binding in hypertrophied prostates from benign prostatic hypertrophy compared to normal tissues, whereas the hypertrophy had little effect on the Kd value.(ABSTRACT TRUNCATED AT 250 WORDS)

Binding, Competitive↗
PubMed1989

Microvascular perfusion during atrial pacing in renal hypertension induced cardiac hypertrophy.

The purpose of this study was to determine if microvascular reserve was recruited during atrial pacing in the hypertrophied myocardium. Hypertrophy was induced by one-kidney, one-clip (1K1C) renal hypertension and compared to uninephrectomized control rabbits 30 days after surgery. Coronary flow was determined by radioactive microspheres. Microvascular perfusion was determined by comparison of fluorescein isothiocyanate-dextran labeled vessels with an alkaline phosphatase stain. Heart rates were not different between groups and all animals were paced 35% above baseline. Baseline coronary flow (176 +/- 44 and 207 +/- 61 ml/min/100 g, control and 1K1C animals) was not altered by pacing in either group. The baseline percent of capillaries perfused was not different between groups (56 +/- 2 and 61 +/- 3%, sham and 1K1C) and the percent perfused increased significantly during pacing for both the non-hypertrophied and 1K1C myocardium (76 +/- 6 and 78 +/- 10%). The baseline percent of the arteriolar bed perfused, was higher in the 1K1C (86 +/- 5%) compared to non-hypertrophied (63 +/- 6%) myocardium. During pacing, the percent of the arteriolar bed perfused increased in non-hypertrophied (89 +/- 14%) but not in the 1K1C myocardium. Although the percent of arterioles perfused did not increase with pacing in the 1K1C myocardium, the capillary reserve was recruited, facilitating the transport of O2 in both the hypertrophied and non-hypertrophied myocardium.

Animals↗
PubMed1985

[Morphologic findings during regression of heart hypertrophy].

The heart is capable of adapting to widely different loads. Increased load will cause hypertrophy with thickening and elongation of the cardiac muscle cells. Beyond the critical heart weight hyperplasia will develop in man. The volume ratio of mitochondria and myofibrils as well as the volume of interstitial tissue and capillaries depends on the type of hypertrophy (training, volume or pressure overload). Hypertrophy will regress when its cause is removed. Training: In experiments with rats 80% of an increase in heart weight caused by swimming was reduced within 14 days after the training program had been stopped. During this time the size of heart muscle cells and the volume ratio of cell organelles had almost completely normalized. From quantitative morphological and biochemical studies, it is supposed that a reduced synthesis but not an obvious increase of catabolism is important in the regression of cardiac hypertrophy. A significant increase in capillary density during the regression period suggests that more time is needed for the regression of capillary length than is required by muscle cells. Training will cause harmonious growth of the left and right chamber wall. During the regression period no quantitative differences of left and right ventricular wall were observed. Pressure overload: Regression of pressure induced hypertrophy is characterized by a reduction of the muscle cell size but not of the amount of collagen in the interstitium. Preliminary studies on pig hearts with an over 100% increase of the weight of their right chamber wall caused by slowly rising pressure load using ameroid constrictors on the A. pulmonalis have shown a 60% reduction of the weight of the right ventricular wall 10 days after removing the constrictor. A reduced mitochondria/myofibrillar ratio becomes normalized. An incomplete or even lacking reduction of the heart weight in rats with spontaneous hypertension (SHR) after therapeutic depression of blood pressure suggests that other factors besides elevated blood pressure are important for inducing hypertrophy in these rats. Valve replacement: An incomplete reduction of heart weight can be observed in patients even after replacement of damaged cardiac valves. Extensive morphological studies on these hearts disclosed recidive infarction or a high degree of cardiac fibrosis as the cause of irreversible hypertrophy. It is still not known whether a case of hypertropied heart with hyperplasia regression will be accompanied by a reduction of the number of myocytes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Catecholamine induced cardiac hypertrophy.

Cardiac hypertrophy was induced in adult female Wistar rats by daily subcutaneous injections of isoproterenol (0.3 mg/kg body weight). Heart weight increased 39% after eight days of treatment. Left ventricular pressure development (positive dP/dt) in hearts four days after hypertrophy induction was significantly increased, while negative dP/dt remained unchanged. RNA polymerase activity in isolated myocyte and nonmyocyte nuclei was stimulated 29 and 23%, respectively 24 h after a single isoproterenol injection. In the myocyte fraction, RNA polymerase activation progressively increased up to four days of treatment and then returned to control values after eight days. In the nonmyocyte nuclear subset, RNA polymerase activity showed no further stimulation and gradually returned to control values after eight days of treatment. Chromatin template function was substantially stimulated in the early stage (one to four days) of hypertrophy in both myocyte and nonmyocyte fractions. Titration of chromatin against a fixed amount of RNA polymerase (5 micrograms) in the presence of rifampicin and heparin showed that less chromatin from hypertrophied hearts was required to saturate the enzyme. These results indicate that both myocyte and nonmyocte chromatin from hypertrophied hearts can support greater enzyme binding than normal chromatin. The alkaline sucrose density centrifugation profile of DNA in myocyte and nonmyocyte chromatin from day 4 hypertrophied hearts was less fragmented. These observations suggest that during the early phase of isoproterenol-induced cardiac hypertrophy, enhanced RNA polymerase activity and chromatin template function play a coordinated role in RNA synthesis. The increased template activity could be due to alterations in chromatin composition which was indicated by the change in their enzyme binding capacity and DNA fragmentation profile.

Animals↗
PubMed1988

[Extreme cardiac hypertrophy in athletes. Morphological and functional echographic study].

Cardiac hypertrophy is an adaptation phenomenon of the heart as a result of increased hemodynamic load due to intense and prolonged training in athletes. This is mainly seen in endurance athletes. In some cases cardiac hypertrophy can mimic hypertrophic cardiomyopathy, specially if hypertrophy is mainly localized at the interventricular septum as compared to the left ventricular free wall. In our study we tried to evaluate the different diagnostic features obtained by echocardiography and clinical examination in a group of 23 athletes with marked hypertrophy (all were participants to the 1984 Olympic Games held in Los Angeles) as compared to a group of 11 sportsmen with non-obstructive hypertrophic cardiomyopathy (HC). Cardiomyopathy was diagnosed on the basis of clinical, echocardiographic and angio-scintigraphic findings. The 23 athletes were selected on the basis of M-Mode and 2D echocardiographic thickness of the interventricular septum (IVS) which was in diastole greater than or equal to 15 mm. They were all asymptomatic, only 4 of the 23 athletes had ECG anomalies due to left axis deviation (LAS) and T wave inversion. Only 4 of the subjects with HC had a family history of HC. ECG changes were the following: T wave inversion (9 subjects), left axis deviation (LAD) (4 subjects), deep Q wave in D2-3, aVF, V5-6 (2 subjects) and low voltage R wave in V5-6 (1 subject). All the athletes had marked hypertrophy of the IVS. Interventricular septum thickness (IVST) was 15.7 +/- 0.6 mm, with a range from 15 to 17.5 mm. Posterior wall thickness (PWT) was 13.7 +/- 1.1 with a range from 12 to 16 mm. The sportsmen with HC had an IVST of 16.2 +/- 3.5 mm and a PWT of 11.3 +/- 1.5 mm. The IVST/PWT ratio was significantly lower (p less than 0.01) in the athletes (1.14 +/- 0.02) when compared to the group with HC (1.4 +/- 0.3). In 7 of the subjects with HC the hypertrophy was mainly localized at the anterolateral segment of the interventricular septum (in 4 of these subjects the hypertrophy involved also the antero-lateral part of the left ventricular free wall).(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗
PubMed1984

[Hypertrophic cardiomyopathy: distribution of the hypertrophy evaluated by bidimensional echocardiography and observations on the genesis of the obstruction].

Two-dimensional echocardiography (2-DE) was performed in 38 patients with hypertrophic cardiomyopathy (HCM) in order to study the distribution of hypertrophy. Its importance in the genesis of the obstruction was evaluated in 26 of these patients who also underwent cardiac catheterization. The hypertrophy was confined to the septum only in 14 patients (37%) and involved both septum and free wall in 24 patients (63%). In the 26 patients who underwent cardiac catheterization, extensive hypertrophy (septum + free wall) was found in 16 of 18 patients with a pressure gradient and in 3 of 8 patients without a pressure gradient. Systolic anterior motion of mitral valve (SAM) was present in all patients with extensive hypertrophy and a pressure gradient. Three patients without a pressure gradient had systolic anterior motion of mitral valve. The two-dimensional echocardiographic finding of systolic cavity elimination was present in 7 of 18 patients with pressure gradient and in none of the patients without. We conclude that in hypertrophic cardiomyopathy: Septal hypertrophy is always present and also involves the free wall in a high percentage of the patients (63%). The data are in agreement with previous observation, apart from isolated free wall hypertrophy which was not seen in our series. The presence of extensive hypertrophy involving the free wall seems to be an essential determinant of a gradient. Systolic anterior motion of mitral valve seems to be the most sensitive (sensitivity = 89%) and cavity elimination the most specific (specificity = 100%) echocardiographic sign of outflow pressure gradient.

Adolescent↗
PubMed1984

Distribution of hypertrophy in obstructive and non-obstructive types of hypertrophic cardiomyopathy.

70 patients with hypertrophic cardiomyopathy were examined by one-dimensional, two-dimensional and pulsed Doppler echocardiography. According to the degree and distribution of hypertrophy in left ventricular (LV) short axis views, the findings were divided into 5 types. In type I, hypertrophy affected only the interventricular septum (10 patients, i.e. 14.2%). In type II, hypertrophy involved besides the septum, also the LV anterior wall (type IIa-26 patients; 37.1%) or lateral wall (type IIb-21 patients; 30.0%). Type III included patients with hypertrophy of the LV posterior wall (3 patients; 4.3%). Six patients (8.5%) had a distinct hypertrophy of the whole apical part of the LV and septum (type IV). Type V was represented by concentric hypertrophy of the LV and septum (4 patients; 5.7%). Hypertrophy of the right ventricular myocardium was found in 6 patients.

Adolescent↗
PubMed1984

[Apical hypertrophy as a part of the morphologic spectrum of hypertrophic cardiomyopathy].

Clinical and morphological features in 10 cases of "apical hypertrophic cardiomyopathy" (apical type) were analyzed and compared with those in classic hypertrophic cardiomyopathy with asymmetric septal hypertrophy (ASH). The hypertrophic pattern of the interventricular septum (IVS) was evaluated on the two-dimensional echocardiographic (2-D) left ventricular (LV) long-axis view. Thirty-one of 70 patients with ASH were characterized by predominant hypertrophy of the basal IVS (Type I). Seventeen patients had predominant hypertrophy of the apical IVS (Type III). Diffuse IVS hypertrophy was noted in 22 patients (Type II). Electrocardiographic similarity was documented between cases with Type III and apical type; that is, a low incidence of abnormal Q waves, a high incidence of giant negative T waves, and frequent absence of Q waves. In Type I and II, abnormal Q waves were frequently observed, while giant negative T waves were rare. On the 2-D LV short-axis view at the papillary muscle level, three groups with ASH revealed similar distributions of myocardial hypertrophy characterized by extension of hypertrophy to the LV anterior free all and papillary muscles. Most cases with apical type had a similar distribution of hypertrophy, but its degree was significantly less severe than that of ASH. Comparison of diastolic LV configurations on left ventriculograms and/or the 2-D apical two-chamber views indicated the morphologic continuity among the three types with ASH and the apical type. Clinical features in cases of the apical type were obviously less severe than those of three groups with ASH, as indicated by a significantly larger proportion of asymptomatic patients (90%), absence of sudden death and rare documentation of malignant ventricular arrhythmias on 24-hours ambulatory electrocardiography. In conclusion, apical type can be categorized as a part of hypertrophic cardiomyopathy with a wide morphologic spectrum rather than the separate disease entity, and it is characterized by giant negative T waves with minimum clinical manifestations.

Cardiac Catheterization↗
PubMed1995

Cardiac hypertrophy impairs recovery from ischaemia because there is a reduced reactive hyperaemic response.

OBJECTIVE: The aim was to investigate whether impaired coronary flow reserve associated with cardiac hypertrophy could significantly limit the flow debt repayment following short periods of coronary occlusion and exacerbate or prolong episodes of myocardial ischaemia. METHODS: Left ventricular hypertrophy was induced in guinea pigs by aortic constriction and the hearts were isolated six weeks later for Langendorff perfusion. Sham operated animals served as controls. The reactive hyperaemic response was studied following various lengths of occlusion of flow and the extent of aerobic and anaerobic metabolism was assessed in each group. RESULTS: Heart weight/body weight ratio was increased by approximately 25% (P < 0.001) with aortic constriction. The reactive hyperaemic flow response in isolated hearts was impaired by hypertrophy in both magnitude (P < 0.05) and duration. The repayment of flow debt was also significantly reduced, suggesting an inadequate recovery of the myocardium following the occlusion. The total amount of O2 consumed by the heart throughout the duration of hyperaemia was less in hypertrophy than in sham operated controls, suggesting a decrease in aerobic metabolism. Total lactate discharge expressed as a ratio of O2 consumed, which provides an estimation of the degree of anaerobic in relation to aerobic metabolism, was greater in hypertrophy than in sham operated controls. CONCLUSIONS: The hypertrophied heart is more vulnerable to brief periods of ischaemia because of an impaired reactive hyperaemic response which results in delayed metabolic recovery. These abnormalities may contribute to the increased morbidity associated with cardiac hypertrophy.

Animals↗