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At least 541 records · Page 30Linked to original sources
PubMed2002

Characteristics of single Ca(2+) channel kinetics in feline hypertrophied ventricular myocytes.

OBJECTIVE: To explore the mechanism underlying the prolongation of action potential and delayed inactivation of the L-type Ca(2+) (I(Ca, L)) current in a feline model of left ventricular system hypertension and concomitant hypertrophy. METHODS: Single Ca(2+) channel properties in myocytes isolated from normal and pressure overloaded cat left ventricles were studied, using patch-clamp techniques. Left ventricular pressure overload was induced by partial ligation of the ascending aorta for 4 - 6 weeks. RESULTS: The amplitude of single Ca(2+) channel current evoked by depolarizing pulses from -40 mV to 0 mV was 1.02 +/- 0.03 pA in normal cells and 1.05 +/- 0.03 pA in hypertrophied cells, and there was no difference in single channel current-voltage relationships between the groups since slope conductance was 26.2 +/- 1.0 pS in normal and hypertrophied cells, respectively. Peak amplitudes of the ensemble-averaged single Ca(2+) channel currents were not different between the two groups of cells. However, the amplitude of this averaged current at the end of the clamp pulse was significantly larger in hypertrophied cells than in normal cells. Open-time histograms revealed that open-time distribution was fitted by a single exponential function in channels of normal cells and by a two exponential function in channels of hypertrophied cells. The number of long-lasting openings was increased in channels of hypertrophied cells, and therefore the calculated mean open time of the channel was significantly longer compared to normal controls. CONCLUSION: Kinetic changes in the Ca(2+) channel may underlie both hypertrophy-associated delayed inactivation of the Ca(2+) current and, in part, the pressure overload-induced action potential lengthening in this cat model of ventricular left systolic hypertension and hypertrophy.

Animals↗
PubMed2001

Thallium-201 myocardial scintigraphy in hypertensive patients with and without left ventricular hypertrophy: a clinical study.

OBJECTIVE: To evaluate the myocardial perfusion in hypertensive patients with and without left ventricular hypertrophy using thallium-201 (201TI) myocardial scintigraphy and explore the mechanism that causes the perfusion abnormalities. METHODS: Thallium-201 myocardial scintigraphy was performed in 85 patients with clinically suspected coronary artery disease to assess the myocardial perfusion status. For patients with myocardial perfusion abnormalities as indicated by the scintigraphy, coronary angiography was ordered within 1 month. RESULTS: The incidence of 201TI myocardial perfusion abnormalities in hypertensive patients with ventricular hypertrophy (85.7%) was significantly higher than that in the normotensive (39.3%, P<0.01) and hypertensive patients not complicated with hypertrophy (61.2%, P<0.05). The semiquantitative score was higher in the hypertensive patients with hypertrophy than in the normotensive (P<0.01) and hypertensive patients without hypertrophy (P<0.05). More hypertensive patients with hypertrophy (9/18) had normal results of coronary angiography than the normotensive (0/13, P=0.044) and hypertensive patients without hypertrophy did (3/19, P<0.05). CONCLUSIONS: A higher rate of 201TI perfusion abnormalities occurs in the hypertensive patients with ventricular hypertrophy, which may be attributed to the pathological changes in the major coronary vessels and to the coronary microvascular diseases as well.

Journal Article↗
PubMed2004

[Comparison of changes in left ventricular gene expression profiles from different cardiac hypertrophy models in rats].

To get insights into the principles of gene expression changes during cardiac hypertrophy, three rat cardiac hypertrophy models were prepared, i.e., suprarenal abdominal aortic stenosis (SRS), arterial-vein fistula (AVF) and continuous jugular vein infusion of norepinephrine (NEi). The cardiac function and structure were analyzed by echocardiograph as well as histological examination. Total RNA of left ventricles was extracted and gene expression profiles were analyzed by cDNA microarray. SRS and NEi induced concentric cardiac hypertrophy and AVF induced eccentric hypertrophy in rats, among which NEi caused obvious cardiac fibrosis. The changes of gene expression profiles were compared comprehensively across different pathologic cardiac hypertrophy models. While gene expression profiles of different cardiac hypertrophy models compared with pairs, parts of the genes involved were found overlapped, and mostly the gene expression changed in the same direction between two models, but some of them changed in the opposite directions. Expression levels of 19 genes were found changed across all cardiac hypertrophy models, and genes relatively regulated in a specific model was also found when comparison of all the three models was carried out. Novel clues for further study might derive from the results mentioned above, and some genes might be the marker genes of cardiac hypertrophy or the targets of therapy.

Animals↗
PubMed1992

[Hypertensive cardiopathy. Functional evaluation during isometric effort after regression of left ventricular hypertrophy].

OBJECTIVE: Echocardiographic evaluation of the response to isometric exercise of hypertensive patients with and without left ventricular hypertrophy. PARTICIPANTS: 28 patients with severe arterial hypertension on long-term follow-up with or without regression of left ventricular hypertrophy on medical therapy; a control group of 10 healthy volunteers. METHODS: Two groups were considered: Group A persistent left ventricular hypertrophy and group B normalization of the left ventricular wall thickness and mass index. The arterial blood pressure and heart rate were evaluated and an echocardiographic record was obtained both at rest and after isometric exercise (maximal effort for 1 to 1.5 minutes). The following echocardiographic data were obtained: left ventricular diameters and thickness of septum and posterior wall during systole and diastole. Volumes, shortening and ejection fractions, cardiac output and index, mass index, end-systolic stress, contractility index and periferal resistance were calculated as usual. RESULTS: During isometric exercise there was a rise in systolic, diastolic and mean arterial pressures and heart rate. Systolic function was normal in all groups at rest. The shortening fraction was not altered in normotensive individuals with isometric exercise. Hypertensive patients showed a significant reduction within normal limits, however. End-systolic stress increased significantly in all groups although the rise was greater in hypertensive patients. The cardiac index rose significantly only in normotensives and hypertensive patients without left ventricular hypertrophy (group B). On the contrary the periferal resistance rose significantly only in hypertensive patients with left ventricular hypertrophy (group A). The contractility index (end-systolic stress/end-systolic volume index) increased significantly only in normotensive and hypertensive patients without left ventricular hypertrophy. CONCLUSIONS: There are functional alterations in hypertensive heart disease which although not evident at rest, can be revealed by isometric exercise. The regression of left ventricular hypertrophy back to normal, sets a trend for normalization of function and cardiac inotropic reserve, suggesting the importance of a complete regression of ventricular hypertrophy.

Adult↗
PubMed1992

[Effect of extent and distribution of left ventricular hypertrophy on clinical aspects and hemodynamics of patients with hypertrophic obstructive cardiomyopathy].

UNLABELLED: The influence of the extent and distribution of the echocardiographically determined left-ventricular hypertrophy was evaluated in respect to clinical symptoms and hemodynamics at rest and under bicycle-exercise. 49 patients with hypertrophic obstructive cardiomyopathy [HOCM] (34 men, 15 women, mean age 43 years, subvalvular gradient after provocation 10-270 mm Hg, ejection fraction greater than 55%) and 10 controls (seven men, three women, mean age 44 years) were investigated. Enddiastolic left-ventricular diameter and basal thickness of the anterior and posterior septum, and the lateral and posterior wall of the left ventricle were echocardiographically measured. The distribution of basal hypertrophy (for the anterior septum and the posterior wall greater than or equal to 15 mm, for the posterior septum and the lateral wall greater than or equal to 17 mm) was classified as type I (1 segment, n = 17), II (2, n = 14) and III (greater than or equal to 3 segments, n = 18), according to Maron et al. (1981). At rest and during symptom-limited bicycle exercise, cardiac index (CI), stroke volume index (SVI), and mean pulmonary capillary wedge pressure (PCWP) were determined at sinus rhythm by a Swan-Ganz-catheter and by the thermodilution method. RESULTS: With increasing hypertrophy, there was a reduction of the left-ventricular enddiastolic diameter. A NYHA-class greater than II was observed in 18% of patients with type-I hypertrophy, in 29% with type II, but in 61% with type III (p less than or equal to 0.05). Of patients with type III, 44% (p less than or equal to 0.05). In type-III hypertrophy the with type I 6% had suffered syncopes; with type II, 14%, and with type III, 44% (p less than or equal to 0.05). In type-III hypertrophy the maximum exercise level (72 +/- 24 Watt) was significantly (p less than 0.05) lower compared with controls (110 +/- 42 W), in type I (99 +/- 35 W), and in type II (100 +/- 45 W). At maximum stress PCWP was significantly increased in types I, II, and III (type I = 22 +/- 8 mm Hg, II = 24 +/- 12 mm Hg, III = 29 +/- 8 mm Hg) compared with controls (8 +/- 4 mm Hg); SVI was significantly lower in type III (49 +/- 13 ml/m2) than in controls (65 +/- 12 ml/m2) and in type I (60 +/- 11 ml/m2); SVI was 60 +/- 17 ml/m2 in type II. At maximum stress, cardiac index was significantly lower in type III (6.2 +/- 2.1 l/min/m2) than in controls (8.9 +/- 2.1 l/min/m2) and in type I (8.4 +/- 1.7 l/min/m2). CONCLUSIONS: In patients with HOCM, severe left-ventricular hypertrophy type III accompanied by a reduced ventricular cavum is associated with more pronounced clinical symptoms, a reduced working capacity and the occurrence of syncopes. In these patients, despite increased filling pressures, the increase in stroke volume and cardiac index are insufficient at stress. Therefore, echocardiographically evaluated left-ventricular hypertrophy and geometry are helpful to estimate the severity of functional disorder in HOCM.

Adult↗
PubMed2006

Time course alterations of myocardial endothelin-1 production during the formation of exercise training-induced cardiac hypertrophy.

Endothelin (ET)-1 is produced by endothelial cells and cardiac myocytes. ET-1 has positive inotropic and chronotropic effects on the heart and causes myocardial cell hypertrophy. Exercise training induces a physiologic cardiac hypertrophy. To study whether myocardial ET-1 is involved in the formation of exercise training-induced cardiac hypertrophy, we investigated time-course alterations of myocardial ET-1 gene expression and ET-1 peptide level in the heart of rats during a formative process of exercise training-induced cardiac hypertrophy. We used the hearts of rats that had been exercise-trained for 4 weeks (4WT) or 8 weeks (8WT) and sedentary control rats for 4 weeks (4WC) or 8 weeks (8WC). Exercise-trained rats performed treadmill running for 5 days/week (60 mins/day). Left ventricular mass index and wall thickness and stroke volume index, measured using echocardiography, in the 8WT group were significantly greater than in the 8WC group, although there were no differences between the 4WC and 4WT groups in these parameters. These results indicated that the 8WT rats developed physiologic cardiac hypertrophy, whereas the 4WT rats did not yet have cardiac hypertrophy. Myocardial ET-1 gene expression and tissue ET-1 concentration in the heart were significantly higher in the 8WT group than in the 8WC group, whereas these values did not differ between the 4WC and 4WT groups. The present study suggests that an alternation of myocardial ET-1 production corresponds with the formation of exercise training-induced cardiac hypertrophy. Therefore, the exercise training-induced change in myocardial ET-1 production may participate in a mechanism of exercise training-induced cardiac adaptation (e.g., cardiac hypertrophy).

Adaptation, Physiological↗
PubMed1987

Role of myocardial hypertrophy in trophic stimulation of indices of sympathetic cardiac innervation.

Indices of cardiac sympathetic innervation have commonly been found depressed in the failing, hypertrophied heart. In contrast, we have recently demonstrated that hemodynamically compensated, very gradually developing right ventricular hypertrophy is associated with an increase in sympathetic nervous markers. The present experiments were performed to corroborate these findings in a model of acutely induced right ventricular hypertrophy, and to further characterize changes in markers of autonomic innervation associated with cardiac hypertrophy. Male guinea pigs underwent either pulmonary artery banding (P) with an acutely constricting ligature, or bilateral stellate ganglionectomy (S), or both (PS). Appropriate sham procedures were performed in animals subjected to only one intervention; controls (C) underwent sham-S and sham-P. Groups of animals were sacrificed at 10 and 20 days after surgery. Cardiac tissues were weighed and subsequently analyzed for activities of tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH), two enzymes catalyzing the biosynthesis of catecholamines (CAs), and of choline acetyltransferase (CAT), a marker of parasympathetic activity, as well as for norepinephrine (NE). S resulted in profound depletions of cardiac NE of 88-92% and in significant decreases in the activities of DBH and TH. Marked right ventricular hypertrophy developed rapidly following P, and was not modified by S. Similar to our previous results, acute right ventricular hypertrophy was associated with moderate increases (10-20%) of sympathetic markers; following S, these increases (of presumably residual sympathetic innervation) were greatly enhanced, amounting to 171% and 105% for NE at 10 and 20 days, respectively. In contrast, sympathetic markers in the left ventricle of stellatectomized animals were not affected by P. Activity of CAT remained unaltered by the experimental interventions. Our experiments indicate that increases in markers of sympathetic innervation may be a common feature of the early, compensated stage of cardiac hypertrophy, regardless of its time course. Sympathetic neural mechanisms do not appear to play a stimulatory or trophic role in the hypertrophic process. Conversely, they seem to be secondary in nature, suggesting a possible stimulatory influence of hypertrophying myocardium on sympathetic cardiac nerves.

Animals↗
PubMed1987

Influence of drug therapy on myocardial hypertrophy in left ventricular failure.

The terminal phases of volume-overload heart failure are characterised by eccentric ventricular hypertrophy. Relatively little attention has been directed to exploring the mechanisms involved in this development. The increase in diastolic wall stress leads to replication of the sarcomeres in series. The hypertrophied myocytes has a defective contractile ability that is due to an intrinsic depression of contractility; this is restored when failure is reversed. The development of appropriate hypertrophy is dependent upon adequacy of the coronary blood supply to the failing myocytes. Reduction of preload and afterload can be expected to be more effective in reducing systolic wall stress, and hence myocardial oxygen demands, in eccentric hypertrophy than in the nonfailing heart with concentric hypertrophy. However, there is no information available on the influence of anti-heart-failure drugs on the myocardial hypertrophy associated with severe volume-overload failure. The presence of such hypertrophy carries an ominous prognosis and may be associated with the high incidence of arrhythmic sudden deaths. The detection of myocardial hypertrophy in the patient with failure emphasises the urgency of adequate reduction of the elevated preload and afterload without impairment of the coronary perfusion gradient.

Cardiomegaly↗
PubMed1989

Reaction patterns of the myocardial interstitium in different models of cardiac hypertrophy--stereological investigations.

Several experimental models of cardiac hypertrophy were investigated in rats: 1. mild hypertrophy induced by physical exercise (18 weeks), 2. mild hypertrophy induced by renovascular hypertension (24 weeks), 3. moderate hypertrophy induced by renovascular hypertension in diabetic and non-diabetic animals (8 weeks), 4. moderate hypertrophy induced by renovascular hypertension in diabetic and non-diabetic animals (12 weeks), 5. moderate hypertrophy induced by thyroxin application (4 weeks), 6. mild hypertrophy in chronic uremia (5/6 nephrectomy, 3 weeks). It is concluded from quantitative stereological parameters of the left ventricular papillary muscles that 1. in hypertrophic hearts myocardial blood flow and oxygen consumption, respectively, rather than the size of muscle fibres determine the capillary supply of the myocardium, 2. interstitial fibrosis occurs in hypertrophy induced by chronic pressure overload and depends on degree and duration of hypertension, 3. the extent of interstitial fibrosis in hypertension is magnified by diabetes mellitus, and 4. the interstitial fibrosis which occurs in chronic uremia is not caused by hypertension.

Animals↗
PubMed1985

[Regression of left heart hypertrophy in arterial hypertension: principles, experimental and clinical findings].

Left ventricular hypertrophy is the consequence of a structural adaptation of the heart in response to the chronic pressure load, leading to a reduction of the increased systolic wall stress. Studies in spontaneously hypertensive rats have shown, that left ventricular hypertrophy can be influenced by various, but not all antihypertensive agents. Alpha-methyldopa, captopril, beta-blockers and calcium channel blockers resulted in reversal of hypertrophy. Treatment with diuretics, hydralazine or minoxidil did not increase or alter degree of myocardial hypertrophy despite normalization of blood pressure. The biochemical profile after reversal of hypertrophy differs according to antihypertensive therapy, i.e. alpha-methyldopa induces an increase in collagen content, whereas captopril does not alter the collagen content of the myocardium. Adrenergic factors play an important role in modulating the response of the heart. In clinical studies the reduction in cardiac mass does not depend solely on the antihypertensive effect on blood pressure levels. There is only a weak correlation between decrease of left ventricular hypertrophy and fall of blood pressure level, as is shown in 12 patients with essential hypertension, treated with captopril over 6 months. The degree of regression of hypertrophy is influenced by stability of blood pressure control (diurnal variations and response to stress are more important than single casual values), neurohumoral response, presence of associated cardiac diseases, cause and severity of hypertension, genetic factors and age. We studied the regression of left ventricular hypertrophy by M-mode-echocardiography in 12 patients with mild or moderate essential hypertension during a 6-month therapy with captopril (50-75 mg p.d.) and hydrochlorothiazide (50 mg p.d.). In 11 of 12 patients captopril treatment resulted in a reduction of LV-mass of 30.9 +/- 15.1% and wall thickness. Peak systolic and endsystolic wall stress decreased significantly (-29.1% and -27.2%, resp.) after blood pressure reduction, but were still slightly elevated. Ejection fraction increased by 5.4% (p less than or equal to 0.05). 6 hypertensive patients treated for 6 months with metoprolol (150 mg p.d.) and hydrochlorothiazide (50 mg p.d.) do not show significant reduction of LV-mass (-6.5%). Peak and endsystolic wall stress were significantly reduced (-33.1% and -11.5%, resp.) as in captopril therapy. In 34 patients with severe hypertension treated with captopril, hydrochlorothiazide and metoprolol over 30 months, we observed a decline in the Sokolow-Lyon-Index from 4.8 +/- 1.1 mV to 3.8 +/- 0.5 mV after 6 months.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

[Progression and regression of heart hypertrophy in arterial hypertension: pathophysiology and clinical aspects].

The criteria of the degree of hypertrophy and dilatation are defined. On this basis, functional and therapeutical regimen of regression of cardiac hypertrophy (prazosin, clonidine, nifedipine) are analyzed in concentric as well as in excentric hypertrophy in patients with arterial hypertension. Regression of cardiac hypertrophy is possible by differentiated pharmacotherapy, e. g., by prazosin, calciumantagonists, clonidine, alphamethyldopa, ACE-inhibitors as well as by combination therapies (beta-receptor blocking agents plus diuretics plus vasodilators). By these therapeutical measurements improvements in ventricular function can be achieved. Coronary reserve can be improved, consecutively the ischemic risk of hypertrophied cardiac muscle may be reduced. By the availability of pharmacotherapeutical regression of cardiac hypertrophy differentiated pharmacotherapy is possible in cardiac hypertrophy in man. Parallel to the regression improvement in ventricular function is possible. It remains still investigated, whether pharmacotherapeutical regression of cardiac hypertrophy is associated with decrease in coronary and late myocardial complications and whether prognosis of hypertensive heart disease can be significantly improved.

Blood Pressure↗
PubMedDate not supplied

Alterations in sarcolemmal Na+-Ca2+ exchange and ATP-dependent Ca2+-binding in hypertrophied heart.

In order to examine changes in Ca2+ transport in heart sarcolemma, cardiac hypertrophy was induced in rabbits by stenosis of the abdominal aorta and hearts were removed 18-20 weeks later; sham-operated normal rabbits were used as controls. Sarcolemmal vesicles were isolated from the left ventricular tissue by a sucrose density gradient method and the membrane composition as well as activities of certain marker enzymes were monitored to determine the purity of control and experimental fractions; Na+-Ca2+ exchange and Ca2+-pump activities were assessed by the Millipore filtration technique. No changes in Ca2+-influx were observed in Na+-loaded vesicles from the hypertrophied hearts when studied in the presence of different concentrations of calcium as well as at different times of incubation. In contrast, Na+-induced Ca2+-efflux from Ca2+-loaded vesicles was enhanced in the hypertrophied heart at different times of incubation and at different concentrations of sodium. ATP-dependent Ca2+-binding activity of sarcolemma from hypertrophied heart, when measured at different times of incubation and at several concentrations of calcium, was more than the control. Minimal but an equal amount of cross contamination was seen in both control and experimental preparations; however, phosphatidylcholine, phosphatidylethanolamine and phosphatidic acid contents were increased in sarcolemma from hypertrophied hearts. These results suggest that the sarcolemmal Ca2+-transport systems may become adapted during the development of hypertrophy for augmenting Ca2+-efflux from the hypertrophied myocardial cell and this may prevent the occurrence of intracellular Ca2+ overload in a stable form of cardiac hypertrophy.

Adenosine Triphosphate↗
PubMed1987

Alterations in the coronary circulation in hypertrophied ventricles.

During the past decade our understanding of the complex interaction between cardiac muscle and coronary vascular growth has increased substantially. Some types of cardiac hypertrophy, for example, left ventricular hypertrophy secondary to hyperthyroidism, are associated with increased coronary vascular growth. However, in most animal preparations of hypertrophy and in several clinical types of hypertrophy of the left and/or right ventricles, pathologic cardiac enlargement impairs the ability of the coronary circulation to allow normal increases and perfusion in response to intense dilator stimuli. In general, clinical studies have demonstrated far more profound abnormalities than studies in experimental animals. These observations provide a plausible explanation of why patients with hypertrophied ventricles often exhibit signs and symptoms of myocardial ischemia in the absence of coronary obstructive disease. The recent observation that experimentally produced left ventricular hypertrophy secondary to renal hypertension augments infarct size and the incidence of sudden lethal arrhythmias has additional implications relevant to the interaction between cardiac hypertrophy and myocardial perfusion. Although coronary reserve is impaired in many types of pathologic hypertrophy, the anatomic or biochemical basis for these observations remains elusive.

Animals↗
PubMed1987

Heart and vessel hypertrophy in hypertension: possibilities of regression.

Fifty-two middle-aged hypertensive males with left ventricular hypertrophy, diagnosed by echocardiography, were divided into two groups; 30 of them were treated with beta-blockers and 22 with methyldopa. Where blood pressure was insufficiently controlled, diuretics and, eventually vasodilating agents, were added to both treatment regimes. During 2 years of follow-up, blood pressure decreased significantly. The greatest decrease was observed during the first 3 months. Echocardiography revealed the greatest decrease in posterior wall and interventricular septal thickness also during the first 3 months. Posterior wall hypertrophy was reversed completely in the next 3 months, while further regression of interventricular septal hypertrophy was continuous during the remaining follow-up period. Left ventricular hypertrophy was reversed completely in 27 (51.9%) probands and remained unchanged in two patients. The regression was incomplete in 23 (44.2%) patients who were more obese and whose left ventricular hypertrophy was initially more pronounced. Regression of hypertrophy was not associated with a deterioration in left ventricular function and was achieved even after the addition of vasodilating drugs. No differences were observed between the treatment groups. The pathogenesis of left ventricular hypertrophy still remains unclear. After 2 years, no changes in peripheral vascular resistance in the forearm were observed at reactive hyperaemia. These results indicate that there might be a delay in the regression of vessel hypertrophy compared with that of the left ventricle.

Adult↗
PubMed1987

Pathophysiological aspects of myocardial hypertrophy.

Heart hypertrophy in response to increased workload is a complex process in which this organ adapts to the environment by increasing the muscle mass in terms of additional contractile units and formation of different types of contractile proteins (myosin isozymes). In addition, augmentation of membrane function with respect to calcium transport activities of sarcolemma and sarcoplasmic reticulum occurs at early stages of cardiac hypertrophy associated with hyperfunction of the myocardium. However, if cardiac hypertrophy is left unattended beyond a certain period, physiological hypertrophy is converted to pathological hypertrophy whereby the cardiac muscle is unable to generate an adequate amount of contractile activity. It appears that the sympathetic nervous system is activated for producing beneficial effects at early stages but an elevated level of sympathetic tone for a prolonged period could result in dysfunction of the cardiac muscle. The transition of physiological hypertrophy to pathological hypertrophy seems to be due to the occurrence of intracellular calcium overload in the myocardial cell as a consequence of defects in the membrane calcium transport systems. It is suggested that careful attention should be paid not only to removal of the stimulus responsible for cardiac hypertrophy but also to lowering sympathetic tone. Efforts should also be made to prevent the occurrence of intracellular calcium overload due to membrane defects.

Animals↗
PubMed1988

[Effect of hypertension on asymmetrical septal hypertrophy: an echocardiographic study].

The effect of hypertension on asymmetrical septal hypertrophy was studied by echocardiography to differentiate idiopathic asymmetrical septal hypertrophy (ASH) from ASH with hypertension. One hundred eight patients with ASH proven by echocardiography were categorized in two groups; 53 patients with hypertension (greater than 160 systolic, greater than 95 diastolic) (hypertensive group: HT) and 55 patients with normal blood pressure (normotensive group: NT). Septal hypertrophy was classified as mid-portion (M-type), diffuse (D-type), and basal (B-type) hypertrophy by the long-axis view, and also diffuse (I-type), anterolateral (II-type), anteroseptal (III-type), and anterior septal (IV-type) by the short-axis view, respectively. Endomyocardial biopsy and left ventriculography were performed in 50 patients (18 hypertensives and 32 normotensives). In the hypertensive group, 45%, 30%, and 25% of cases had diffuse, basal and mid-portion hypertrophy, respectively. There was no case in the basal hypertrophy whose biopsy findings were compatible with hypertrophic cardiomyopathy. In the normotensive group, 78% and 22% of patients had midportion and diffuse hypertrophy, respectively, but none of them had the basal hypertrophy. Type IV was seen in only six patients in the normotensive group.

Adult↗
PubMed1982

Improved tolerance to ischemia in hypertrophied myocardium by preischemic enhancement of adenosine triphosphate.

In prior studies from this laboratory to determine the mechanisms whereby hypertrophied myocardium is more sensitive to ischemic injury than normal myocardium, it was demonstrated that hypertrophied rat hearts have lower basal high-energy phosphate levels and develop ischemic contracture sooner than normal myocardium. The purposes of this study were (1) to determine if the decrease in myocardial adenosine triphosphate (ATP) was associated with the increased rate of ischemic contracture and (2) to determine if arrest and perfusion of hypertrophied myocardium prior to the ischemic interval would allow recovery of high-energy phosphate stores and improve tolerance to ischemia. ATP levels were measured in isolated normal and hypertrophied rat hearts during (1) control nonworking Langendorff perfusion, (2)2 minutes of potassium chloride-arrested perfusion (30 mEq/L), or (3) 15 minutes of potassium chloride-arrested perfusion (30 mEq/L). Both groups were then made globally ischemic (37 degrees C) and the time to ischemic contracture recorded. Hypertrophied hearts were produced by permanent banding of the ascending aorta and confirmed by left ventricular (mg) body weight (gm) ratios (normal, 1.95 wet, p less than 0.05). After 2 minutes of mechanical arrest the time to ischemic contracture was increased 75% +/- 10% in normal and 44% +/- 4% in hypertrophied hearts. After 15 minutes of mechanical arrest with perfusion, hypertrophied myocardium re-established normal ATP levels and increased its time to ischemic contracture by 130% +/- 7%. These studies suggest that during potassium chloride arrest, additional preischemic metabolic recovery is possible by hypertrophied myocardium and leads to increased tolerance to ischemia beyond that accomplished by cessation of mechanical activity alone. This effect is seen only to a minor degree in normal myocardium.

Adenosine Triphosphate↗
PubMed1981

[Contribution of M-mode echocardiography and myocardial scintigraphy for study of ECG pattern of left ventricular hypertrophy with giant negative T waves (author's transl)].

Eight normotensive patients with electrocardiographic criteria for left ventricular hypertrophy with giant negative T waves were studied with Thallium-201 imaging and M-mode echocardiography. In all the patients Thallium scanning demonstrated increased thickness of the left ventricular walls. In five of the above cases areas of increased uptake were noted in the apical region which had increased thickness as compared to the rest of the left ventricular wall. Echocardiography showed in one subject obstructive hypertrophic myocardiopathy and in another two asymmetric septal hypertrophy. In the remaining patients there was always present septal and posterior wall hypertrophy. Reliable echocardiograms of the apex were done in five subjects and in these hypertrophy was noted. The results of the two techniques were compared and correlated clinically and with the literature. The authors conclude in agreement with other studies that the picture of electrocardiographic left ventricular hypertrophy with giant negative T waves is indicative of hypertrophic myocardiopathies. Specifically, for us, the apical hypertrophy may be the only feature of the myocardiopathy or be part of a generalized left ventricular hypertrophy which is usually asymmetric septal hypertrophy.

Adult↗