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PubMed1994

Possible involvement of endothelin-1 in cardiac hypertrophy.

In an attempt to ascertain a possible involvement of endothelin-1 (ET-1) in the development of cardiac hypertrophy induced by hemodynamic overloads in vivo, the expression of prepro ET-1 mRNA in the cardiac tissue and the plasma level of ET-1 were determined in rats undergoing various treatments for inducing cardiac hypertrophy. One week after aortic banding (AB), the rat exhibited left ventricular hypertrophy characterized by ventricular wall thickening, i.e. concentric hypertrophy. In contrast, the aortic regurgitation (AR) produced left ventricular enlargement without wall thickening 1 week after the operation, i.e. eccentric hypertrophy. Monocrotaline treatment (s.c.) also caused marked hypertrophy in the right ventricle (concentric hypertrophy) 3 weeks later, which was accompanied by a severe pulmonary hypertension (MCT-PH). A Northern blot analysis revealed that AB and MCT-PH markedly increased the expression of prepro ET-1 mRNA in the left and right ventricles, respectively. The rats with MCT-PH but not with AB displayed a significant higher level in their plasma ET-1 levels compared with control animals. In contrast, the rats undergoing AR surgery exhibited no significant elevation in either prepro ET-1 mRNA in the heart or the plasma ET-1 concentration. The results of the present study suggest that ET-1 is involved at least in part in the development of concentric but probably not eccentric cardiac hypertrophy induced by hemodynamic overloads.

Animals↗
PubMed1993

Contractile properties of skinned fibers from hypertrophied skeletal muscle.

We have previously shown deficits in specific tension (N.cm-2) in whole hypertrophied skeletal muscle (18-30%). The purpose of the present study was to determine if this intrinsic deficit exists in chemically skinned, hypertrophied single fibers, and also to measure their Ca2+ sensitivity. One group of rats (N = 4) had bilateral surgical ablation of the gastrocnemius and soleus muscles, and another group (N = 4) had the gastrocnemius and plantaris muscles ablated to induce hypertrophy in the plantaris and soleus muscles, respectively. Thirty days after surgery five fibers were dissected and analyzed from each of eight muscles per group, including control muscles. In hypertrophied plantaris and soleus muscles, fiber cross-sectional area (CSA) was 20% and 29% greater, respectively, than control values. Maximal Ca2+ activated tension (Po, pCa 4.5) was 15% greater in hypertrophied plantaris fibers and 18% greater in hypertrophied soleus fibers compared with respective control values (P < 0.05). Therefore, Po expressed per fiber CSA was slightly depressed (3-8%) in both plantaris and soleus fibers (P < 0.05). Regarding Ca2+ sensitivity, the Ca2+ concentration to elicit 50% of Po (i.e., pCa50) was significantly lower in hypertrophied soleus (58%) and plantaris (29%) fibers. This leftward shift in the force-pCa curve reflects greater Ca2+ sensitivity in hypertrophied fibers. Since the single fiber Po/CSA was only slightly decreased, these data suggest that during tetanic stimulation of whole muscle Ca2+ delivery to the contractile apparatus may be impaired.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

[Cardiac hypertrophy in hypertension--clinical significance and possibilities of control].

Left ventricular hypertrophy constitutes an essential risk factor for sudden death, myocardial infarction and heart failure. The death rates of patients with ECG-demonstrated cardiac hypertrophy are 4.8 times as high as those of healthy subjects. Cardiac hypertrophy is associated with a substantially increased incidence of ventricular arrhythmias. The condition is treatable in most patients. While the most effective group of drugs for controlling cardiac hypertrophy are ACE inhibitors; methyldopa, calcium antagonists, and beta-blockers have also proved useful in the management of cardiac hypertrophy in hypertension. Diuretics other than indapamide are not appropriate for treating cardiac hypertrophy. An additional benefit of ACE inhibitor administration is they can favourable affect increased levels of collagen in the hypertrophic myocardium. The prognosis of hypertensive patients, whose treatment has lead to regression in cardiac hypertrophy in hypertension, is markedly better than that of patients in whom regression fails to be achieved. A role in the development of cardiac hypertrophy in hypertension, in addition to the blood pressure level, is played by a number of mechanisms; it is the genetic factor which has received most attention recently. As the prognosis of hypertrophic patients has been found to correlate more closely with left ventricular weight, determined by echocardiography, than with blood pressure, echocardiography should be employed more often in the future to help optimize antihypertensive therapy.

Death, Sudden, Cardiac↗
PubMed1997

Alternative splicing and cycling kinetics of myosin change during hypertrophy of human smooth muscle cells.

We investigated in vivo expression of myosin heavy chain (MHC) isoforms, 17 kDa myosin light chain (MLC17), and phosphorylation of the 20 kDa MLC (MLC20) as well as mechanical performance of chemically skinned fibers of normal and hypertrophied smooth muscle (SM) of human myometrium. According to their immunological reactivity, we identified three MHC isoenzymes in the human myometrium: two SM-MHC (SM1 with 204 kDa and SM2 with 200 kDa), and one non-muscle specific MHC (NM with 196 kDa). No cross-reactivity was detected with an antibody raised against a peptide corresponding to a seven amino acid insert at the 25K/50K junction of the myosin head (a-25K/50K) in both normal and hypertrophied myometrium. In contrast, SM-MHC of human myomatous tissue strongly reacted with a-25K/50K. Expression of SM1/SM2/NM (%) in normal myometrium was 31.7/34.7/33.6 and 35.1/40.9/24 in hypertrophied myometrium. The increased SM2 and decreased NM expression in the hypertrophied state was statistically significant (P < 0.05). MHC isoform distribution in myomatous tissue was similar to normal myometrium (36.3/35.3/29.4). In vivo expression of MLC17a increased from 25.5% in normal to 44.2% in hypertrophied (P < 0.001) myometrium. Phosphorylation levels of MLC20 upon maximal Ca(2+)-calmodulin activation of skinned myometrial fibers were the same in normal and hypertrophied myometrial fibers. Maximal force of isometric contraction of skinned fibers (pCa 4.5, slack-length) was 2.85 mN/mm2 and 5.6 mN/mm2 in the normal and hypertrophied state, respectively (P < 0.001). Apparent maximal shortening velocity (Vmax(appt), extrapolated from the force-velocity relation) of myometrium rose from 0.13 muscle length s-1 (ML/s) in normal to 0.24 ML/s in hypertrophied fibers (P < 0.001).

Adult↗
PubMed1989

Effects of chronic infusion of norepinephrine on cardiac structure, function, and biochemistry: physiologic versus pathologic hypertrophy.

Ventricular hypertrophy should be divided into at least physiologic and patholgic states in order to clarify structural and functional clinical alterations. The elucidation of the structural, functional, and biochemical mechanisms of ventricular hypertrophy is vital to designing effective preventive and therapeutic measures for the hypertensive patient. Tissue markers may help differentiate pathologic from physiologic hypertrophy. Studies have established the concept that norepinephrine may be a myocardial cellular hypertrophying hormone. The studies ranged from the direct application of norepinephrine to isolated myocardial cells to the chronic subhypertensive infusion of norepinephrine into the conscious, free-roaming dog. Norepinephrine infusion can produce physiologic ventricular hypertrophy or a pathologic state of hypertrophic cardiomyopathy, the former by a three- to four-month infusion and the latter by an infusion of more than six months. The biochemical effect of subhypertensive infusion of norepinephrine was studied prior to the production of ventricular hypertrophy, thereby permitting the elucidation of the mechanism of the hypertrophic process. The biochemical stimulus for the production of myocardial cellular hypertrophy is postulated to be a diminution of cyclic AMP and a stimulation of alpha-1 receptors. Because the ventricular septum has the highest content of adenylate cyclase, which does not increase with cyclic AMP, these changes are postulated to be the biochemical basis for septal hypertrophy in the disease entity hypertrophic cardiomyopathy. A unique conscious-canine model for the production of a myocardial infarction capable of creating a controlled localized occlusion of the coronary artery is presented.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Calcium overload during reperfusion is accelerated in isolated hypertrophied rat hearts.

In this study, calcium overload during reperfusion and the severity of morphologically evident ischemic myocardial injury were compared in hypertrophied and normal hearts. Hypertrophied hearts isolated from rats where a clip had been placed on the proximal thoracic aorta for 6 weeks were compared to those from sham-operated rats in an isolated state perfused with Krebs-Henseleit buffer containing 3% albumin, 1.2 mM palmitate and 11 mM glucose. The isolated hearts were exposed to global, no-flow, normothermic ischemia following potassium arrest and were reperfused. Following ischemia and reperfusion, left ventricular end diastolic pressure was increased (39 +/- 7 v 13 +/- 2 mmHg, P < 0.05), and percentage recovery of left ventricular systolic function was decreased (34.4 +/- 8.9 v 77.1 +/- 6.3% P < 0.05), in hypertrophied hearts compared to control hearts. Calcium overload during reperfusion was two and one-half times greater in the hypertrophied hearts than in the control hearts and showed significant relationships with recovery of left ventricular systolic function (r = -0.86, P < 0.001) and left ventricular end diastolic pressure (r = 0.78, P < 0.005). Myocardial energy charge did not differ between the two groups at the end of reperfusion. Ischemic myocardial injury was quantitated morphologically by point counting techniques in a comparable series of control and hypertrophied hearts. After ischemia, hearts were either exposed to a monoclonal antimyosin antibody to identify and measure irreversibly injured myocardium by light microscopy or fixed by perfusion with 2.5% glutaraldehyde to quantitate the morphologic changes ultrastructurally. Control and hypertrophied hearts were not significantly different in severity of myocardial injury due to ischemia as assessed morphologically. Thus, the data suggest that calcium overload during reperfusion plays a significant role in post-ischemic left ventricular dysfunction of the hypertrophied heart. The accelerated calcium overload that occurs in the hypertrophied rat heart during reperfusion cannot be explained by differences in severity of myocardial injury during ischemia which indicates that other mechanisms are responsible.

Animals↗
PubMed1996

Aging, cardiac hypertrophy and ischemic cardiomyopathy do not affect the proportion of mononucleated and multinucleated myocytes in the human heart.

The current investigation was designed to evaluate whether the proportion of mononucleated binucleated, trinucleated and tetranucleated myocytes varies in the left ventricle, interventricular septum and right ventricular free wall with aging, cardiac hypertrophy and ischemic cardiomyopathy. In addition, the number and dimensional properties of myocytes were measured to determine whether a relationship existed between myocyte size and number, and organ hypertrophy. For this purpose, 72 normal hearts were obtained from individuals who died from causes other than cardiovascular disease and compared with 81 hypertrophied hearts and 95 with ischemic cardiomyopathy. The age interval examined varied from 26 to 93 years. The analysis of enzymatically dissociated myocytes in control left ventricles demonstrated that mononucleated, binucleated, trinucleated, trinucleated and tetranucleated myocytes comprised 74%, 25.5%, 0.4% and 0.1% of the entire myocyte population. Similarly, mononucleated myocytes constituted the prevailing cell population of the interventricular septum and right ventricular free wall. Aging, myocardial hypertrophy and ischemic cardiomyopathy did not change the percentage of mononucleated and multinucleated myocyte in the ventricular myocardium. Cardiac hypertrophy and ischemic cardiomyopathy were characterized by comparable increase in myocyte size in spite of a significant difference in the magnitude of myocardial hypertrophy. Myocyte number was increased in hypertrophied hearts, whereas myocyte cell loss occurred in ischemic cardiomyopathy. In conclusion, aging, cardiac hypertrophy and ischemic cardiomyopathy do not alter the fractions of mononucleated and multinucleated myocytes in the myocardium.

Adult↗
PubMed1997

Altered expression of atrial natriuretic peptide and contractile protein genes in hypertrophied ventricle of JVS mice with systemic carnitine deficiency.

To characterize cardiac hypertrophy in juvenile visceral steatosis (JVS) mice with systemic carnitine deficiency, we investigated how the hypertrophy develops and whether it is associated with altered expression of any specific genes, especially atrial natriuretic peptide (ANP) and contractile protein genes, in the hypertrophied ventricle. Cardiac hypertrophy in JVS mice became apparent at 10 days after birth and progressed during development. The hypertrophy was observed in the ventricles but not in the atria. ANP mRNA was more intensively expressed in JVS ventricles than in control even at 5 days. Carnitine administration ameliorated the cardiac hypertrophy and suppressed the augmentation of ANP mRNA in the ventricles. Isoform change of expression of alpha-actin genes from cardiac to skeletal was seen in the ventricles of JVS mice at 2 weeks. There was no difference in the ratio of beta-myosin heavy chain mRNA to alpha-myosin heavy chain mRNA between control and JVS mice at 5 days, but at 2 weeks the ratio was significantly lower in JVS mice than in control. These results suggest that the molecular characteristics of cardiac hypertrophy caused by carnitine deficiency are different from those of cardiac hypertrophy caused by aortic constriction.

Actins↗
PubMed1992

Left ventricular hypertrophy regression during antihypertensive treatment.

For more than 20 years hypertrophy regression has been in the focus of hypertension research. Many studies in animals have shown impressive reduction of left ventricular hypertrophy after medical treatment of hypertension. The most important result seems to be that hypertrophy can be almost completely reversed in young animals, whereas in older animals regression of left ventricular hypertrophy appears to be less complete. Hypertrophy regression in man seems much more difficult to prove. The direct correlation between left ventricular muscle mass and ECG changes has been disappointing in many studies. Echocardiography is able to show a comparatively good impression of left ventricular muscle mass and therefore can also demonstrate regression of left ventricular hypertrophy within its methodological limits. There is no doubt that today magnetic resonance imaging has by far the best imaging quality of all the clinical methods and is able to demonstrate both hypertrophy and its regression with incomparable accuracy. In the present clinical study hypertrophy regression has been demonstrated after 6 months of treatment with Carvedilol.

Adrenergic beta-Antagonists↗
PubMed1994

Reduction of calcium-independent transient outward potassium current density in DOCA salt hypertrophied rat ventricular myocytes.

Saline-drinking, left-nephrectomized rats made hypertensive by deoxycorticosterone acetate (DOCA) pellet implantation at the time of surgery develop a cardiac hypertrophy, which becomes maximal after 6-7 weeks. The hypertrophy results in a marked increase in the amplitude and duration of both the early and the late component of the ventricular action potential plateau recorded in the isolated perfused rat heart. The 4-aminopyridine(4-AP)-sensitive calcium-independent transient outward potassium current was markedly depressed in hypertrophied ventricular myocytes resulting in a highly significant decrease in current density (from 19.9 +/- 3.5 to 6.4 +/- 3.1 pA/pF at +60 mV). Activation/voltage and steady-state inactivation/voltage relationships were moderately although non-significantly shifted towards negative potentials. The steady-state outward current measured at the end of 1-s depolarizing pulses was not significantly changed in hypertrophied myocytes. 4-AP induced a smaller increase in plateau amplitude and duration in hypertrophied rather than in control hearts, a point that is well explained by the depression of the transient outward current resulting from hypertrophy. We also demonstrated that a complete recovery of both cell capacitance and transient outward current amplitude occurs in myocytes from saline-drinking rats studied 13 weeks after DOCA pellet implantation, showing that hypertrophy regresses as a result of pellet elimination. Several mechanisms can be involved in the observed phenomena, including the possibility that the expression of potassium channels responsible for the transient outward current is not enhanced by hypertrophy in contrast with what occurs in the case of calcium channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMedDate not supplied

In situ mitochondrial function in volume overload- and pressure overload-induced cardiac hypertrophy in rats.

OBJECTIVES: Little comparative information is available on mitochondrial function changes during experimentally-induced hypertrophy. Respiratory control mechanisms are not exactly the same in situ and in isolated mitochondria. This study assessed in situ mitochondrial function in two myocardial hypertrophy models. METHODS: Cytochrome aa3 (Cytaa3) and myoglobin (Mb) absorption changes were monitored in isolated rat hearts using dual wavelength spectrophotometry (Cytaa3: 605-630 nm, Mb: 581-592 nm). Hypertrophy was induced by creation of an aortic stenosis or of an aorto-caval fistula. Optical monitoring was performed on diastole-arrested perfused hearts using the sequence O2 perfusion, N2 perfusion during 4 min, and reoxygenation. The plateaus of the Cytaa3 and Mb curves were used to quantify oxidation-reduction and oxygenation levels. Respiratory kinetics were characterized by the slopes of transition phase curves. RESULTS: Myoglobin oxygenation was comparable in the hypertrophied and control hearts. However, Cytaa3 oxidation-reduction levels in the hypertrophied hearts showed a shift towards greater reduction in comparison with the controls (controls: 0.580 +/- 0.008 DO605/DO630 nm, n = 34; fistula: 0.530 +/- 0.023, n = 23; stenosis: 0.522 +/- 0.016, n = 20, p < 0.001). The rate of Cytaa3 reduction and the rate of myoglobin deoxygenation were significantly accelerated (p < 0.005) in the volume overload group (0.507 +/- 0.043, n = 23), whereas the respiratory rate in the pressure overload group (0.389 +/- 0.034, n = 20) was comparable to that in the control hearts (0.358 +/- 0.026 delta DO 605 nm/DO630 nm.min-1, n = 34). CONCLUSION: We found mitochondrial function alterations in both volume overload- and pressure overload-induced cardiac hypertrophy, despite adequate cytosol oxygenation. The patterns of these alterations differed: the redox state showed a shift of similar magnitude toward greater reduction in both models, but the respiratory rate was increased in the volume-overloaded hearts and unchanged in the pressure-overloaded hearts. The modification in the oxidation-reduction state suggested that overload hypertrophy may induce changes in the metabolism of the myocardium, which may, in turn, load to persistent modifications in mitochondrial function. The differences between the two models suggest that adaptation to hypertrophy-inducing events exists at the level of the mitochondrion.

Absorption↗
PubMedDate not supplied

A biphasic change in contractile proteins during the development of cardiac hypertrophy in pigs.

A non-failing hypertrophy of the left ventricle was produced in the pig heart by supravalvular banding of aorta for 4, 8 and 12 weeks and the myosin and myofibrillar adenosine triphosphatase activities were measured. A significant increase in myosin Ca2+-ATPase activity was seen at 4 weeks of hypertrophy, but at 8 and 12 weeks this activity was significantly decreased compared to sham control. Similar changes were also seen in actin-activated myosin ATPase activities at 4, 8 and 12 weeks of hypertrophy. There were no changes in the K+- and NH4+-EDTA-stimulated ATPAse activities of myosin. Basal ATPase activities of myofibrils were decreased at 4 and 8 weeks of hypertrophy and there was no change in this activity at 12 weeks of hypertrophy. Ca2+ stimulated ATPase activity of myofibrils was significantly increased at 4 weeks, normal at 8 weeks and significantly reduced at 12 weeks of hypertrophy. The changes in ATPase activities were not due to any alterations of proteins by high concentrations of salts during the purification of myosin. The non-hypertrophied right ventricle from the banded animals did not show any change in the basal or Ca2+ stimulated myofibrillar ATPase activities. It is suggested that hypertrophy of the myocardium is accompanied by specific changes in the enzyme activities of the contractile proteins and the biphasic responses may correlate with the functional state of the myocardium subjected to a chronic increase in pressure.

Adenosine Triphosphatases↗
PubMed1979

Effects of cardiac hypertrophy secondary to hypertension on the coronary circulation.

For many years clinicians have suspected that hypertrophied ventricles have an inadequate coronary circulation. Recent studies have confirmed early observations that flow per gram in hypertrophied ventricles is normal at rest. However, coronary vascular resistance is greatly increased when hypertension is the cause of left ventricular hypertrophy. Studies that have employed labeled microspheres to assess regional myocardial perfusion have shown that the transmural distribution of myocardial perfusion is often abnormal in dogs with left ventricular hypertrophy. In addition, studies of cardiac hypertrophy in many animal models have shown that maximal coronary vasodilatation is limited substantially. Furthermore, when hypertrophied hearts are subjected to a physiologic stress that induces coronary vasodilatation, endocardial underperfusion occurs frequently. Thus, studies in animals suggest that cardiac hypertrophy adversely affects the coronary circulation. The availability of new techniques for estimating phasic and transmural coronary blood flow in man should make it possible to extend these studies to patients with cardiac hypertrophy.

Adenosine↗
PubMed1983

Left atrial abnormality as an electrocardiographic criterion for the diagnosis of left ventricular hypertrophy in the presence of right bundle branch block.

Left atrial (LA) abnormality determined from precordial lead V1 was assessed by 2 observers as a criterion of left ventricular (LV) hypertrophy in the presence of right bundle branch block (BBB) in 23 patients. The presence of LV hypertrophy was confirmed from a postmortem cardiac partition technique and defined at 2 levels of confidence: probable and definite hypertrophy. Observers reliably differentiated between the hypertrophied and normal-sized ventricle in the presence of right BBB by using LA abnormality as an electrocardiographic criterion. When defined as definite hypertrophy, observer 1 correctly identified LV hypertrophy in 78% of the cases and observer 2 in 67% of the cases. False-positive results were present in 21% of cases by observer 1 and 14% by observer 2. Comparable results were achieved when a definition of probable hypertrophy was used. Observer performance of recognition of LA abnormality in this study was satisfactory with 91% agreement between observers. Our results are comparable and in some instances superior to conventional criteria commonly recommended to diagnose LV hypertrophy on the electrocardiogram without right BBB.

Aged↗
PubMed1987

Relation between extent of left ventricular hypertrophy and occurrence of ventricular tachycardia in hypertrophic cardiomyopathy.

This study was undertaken to determine whether the occurrence of ventricular tachycardia (VT) in patients with hypertrophic cardiomyopathy (HC) is related to the magnitude and extent of left ventricular (LV) hypertrophy. Extent of LV hypertrophy was assessed using 2-dimensional echocardiography in 30 patients with HC in whom VT had been documented on 24-hour ambulatory electrocardiographic (ECG) monitoring, and the extent of LV hypertrophy in these patients was compared with that of a control group of 61 patients with HC who had normal ambulatory ECG recordings. Severe LV hypertrophy, involving at least 3 of the 4 LV segments, occurred significantly more often in patients with documented VT (16 of 30, 53%) than in those with normal ambulatory ECG findings (13 of 61, 21%; p less than 0.002). Conversely, mild LV hypertrophy, involving only 1 LV segment, occurred significantly less often in patients with VT (5 of 30, 17%) than in the control subjects (32 of 61, 52%; p less than 0.001). Moderate LV hypertrophy, involving 2 of the 4 LV segments, occurred about as frequently in patients with VT (9 of 30, 30%) as in patients with normal ambulatory ECG findings (16 of 61, 26%; p greater than 0.05). In addition, the LV wall thickness index, a quantitative measure of overall extent of LV hypertrophy, was also significantly higher (thereby indicating a greater magnitude of hypertrophy) in patients with documented VT (72 +/- 17 mm) than in those with normal ambulatory ECG recordings (61 +/- 14 mm; p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Population implications of electrocardiographic left ventricular hypertrophy.

Left ventricular (LV) hypertrophy on the electrocardiogram is an ominous harbinger of cardiovascular disease in the general population markedly increasing the risk of coronary heart disease, cardiac failure, stroke and peripheral arterial disease. This contribution to risk exceeds that of the often accompanying hypertension. Once overt coronary disease occurs, electrocardiographic LV hypertrophy also further escalates risk of cardiovascular morbidity and mortality. The risk associated with electrocardiographic LV hypertrophy is particularly great when repolarization abnormality is present. Electrocardiographic LV hypertrophy and silent electrocardiographic myocardial infarction are similar in evolution and prognosis. LV hypertrophy is an important predictor of risk of cardiac failure; the electrocardiographic manifestation of LV hypertrophy predisposes to cardiac failure more than x-ray cardiac enlargement. Electrocardiographic LV hypertrophy heralds the onset of serious cardiovascular disease and premature mortality despite lack of associated symptoms. The serious prognosis of this abnormality warrants vigorous preventive management. More prospective data are needed comparing the prognosis of echocardiographic anatomical hypertrophy with that diagnosed by electrocardiography.

Adult↗
PubMed1989

Relation of electrocardiographic abnormalities to evolving left ventricular hypertrophy in hypertrophic cardiomyopathy during childhood.

Patients with hypertrophic cardiomyopathy (HC) often show substantial increases in left ventricular (LV) wall thickness or even de novo development of LV hypertrophy during childhood. To determine the utility of the electrocardiogram in reflecting such changes in LV mass, serial 12-lead electrocardiograms and 2-dimensional echocardiograms were analyzed in 38 children with HC. The period of evaluation ranged from 3 to 8 years (mean 5.5). Between the initial and most recent clinical evaluations, precordial and standard lead voltages did not change significantly in the study patients, including those showing evolution of LV hypertrophy by 2-dimensional echocardiography; furthermore, only 9 of the 38 patients (23%) showed any substantial change in the overall electrocardiographic pattern. However, the magnitude of electrocardiographic voltages at initial evaluation (age 11 +/- 4 years) showed a significant correlation with the extent of LV hypertrophy at the most recent evaluation as assessed by echocardiography (at age 16 +/- 4 years) (r = 0.65, p less than 0.001). Of note, each of the 7 patients who developed LV hypertrophy during the period of observation had distinct electrocardiographic abnormalities at the initial evaluation that preceded the appearance of LV hypertrophy on the echocardiogram. In conclusion, in children with HC and evolving LV hypertrophy, the electrocardiogram showed little change during the period of observation. However, electrocardiographic abnormalities may be the initial manifestation of HC, appearing even before LV hypertrophy is detectable by echocardiography. Hence, in patients with HC the electrocardiogram may provide advance evidence of morphologic changes that will subsequently occur and may describe the magnitude of LV hypertrophy ultimately achieved an average of 5 years later.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Diversity of patterns of hypertrophy in patients with systemic hypertension and marked left ventricular wall thickening.

In selected patients with systemic hypertension it may be difficult to ascertain whether left ventricular (LV) hypertrophy is a secondary end-organ consequence of long-term elevations in blood pressure or, alternatively, a manifestation of a coexistent primary hypertrophic cardiomyopathy. To address this issue and better characterize LV hypertrophy in systemic hypertension, 2-dimensional echocardiography was used to define the patterns of LV hypertrophy in 102 patients with sustained systemic hypertension and marked degrees of wall thickening. Patients ranged in age from 31 to 88 years (mean 61) and were predominantly female (58%); all were black. By selection, each patient had a maximal LV wall thickness of greater than 15 mm (range 16 to 29). Distribution of hypertrophy was judged to be symmetric (i.e., concentric) in most patients (67 of 102, 66%). However, a substantial proportion (35 patients, 34%) demonstrated nonuniform, asymmetric patterns of hypertrophy in which at least 1 segment of the LV wall was at least 1.5 times the thickness of any other. In these 35 patients, the distribution of hypertrophy was similar to that characteristic of the morphologic spectrum of hypertrophic cardiomyopathy, with thickening of portions of both the ventricular septum and free wall in 16 patients, anterior and posterior ventricular septum alone in 11 patients and segmental involvement of only the anterior ventricular septum in 8. Patients with asymmetric patterns of wall thickening did not differ from the patients with symmetric hypertrophy with regard to age, sex or clinical findings. Asymmetric LV hypertrophy appears to represent an important feature of the morphologic spectrum of severe hypertensive heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗