Although some studies suggest that complement activation is involved in the development of acute myocardial infarction, there has been little convincing evidence of a change in the complement system in patients suffering from myocardial infarction. In this study circulating levels of C3a, C3, C4 and the total hemolytic complement titer (CH50) were serially measured in 12 patients with acute myocardial infarction up to 10 days after an attack. The plasma C3a level was greatly elevated throughout the post-attack observation period. The C3, C4 and CH50 levels were significantly increased above those controls on days 8, 9 and 10 after infarction. These findings indicate that there is complement activation in patients with acute myocardial infarction, and suggest a pathogenetic role for complement activation in the development of myocardial damage after infarction.

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To examine the electrophysiologic characteristics of paroxysmal atrial fibrillation (PAF), we studied intra-atrial conduction delay and fragmented atrial activity during premature stimulation of high right atrium in the following four groups: Group I (n=25), patients without PAF and without sick sinus syndrome (SSS); Group II (n=22), patients with PAF but without SSS; Group III (n=10), patients without PAF and with SSS: Group IV (n=6), patients with PAF and SSS. Intra-atrial conduction delay was the increase in the interval (from the stimuli to the coronary sinus electrogram) observed with early premature beats⩾20 ms compared with that of basic rhythm. Fragmented atrial activity was defined as disorganized atrial activity⩾150% of the duration of high atrial activity of basic beats recorded. The conduction delay zone (CDZ) and fragmented atrial activity zone (FAZ) were significantly wider in Groups II, III and IV than in Group I. There were no significant differences in either CDZs or FAZs among Groups II, III and IV. Thus, the widening of CDZs and/or FAZs are characteristic of PAF and SSS. CDZ and FAZ may be good indices of development of PAF in patients without SSS.

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In 30 consecutive hypertrophic cardiomyopathy (HCM) patients who eventually died and 50 who survived, morphologic and functional changes in the heart during a follow-up period of an average of 3.9 years were echocardiographically evaluated. Echocardiographic indices were compared among 5 groups of patients with HCM, consisting of 4 groups of patients who eveatually died (SD: 17 patients who suffered sudden death, ED: 4 who died of embolism, HF: 4 who died of congestive heart failure, NC: 5 who died of a non-cardiac event) and 1 group of patients who survived with nondilated left ventricle (S: 50 patients). These indices at the last evaluation before death were compared with histopathological findings of left ventricles in 12 autopsied patients. At the initial evaluation ED and HF patients had a larger left ventricular end-diastolic dimension (LVDd), and HF patients had a smaller percent fractional shortening (%FS) and a slower normalized rapid filling rate (nRFR: mean rapid filling rate/LVEDV) than S patients, but these indices shoed no differences between SD and S patients. During follow-up, no echocardiographic indices changed in S patients, but LVDd was increased and %FS and nRFR were decreased i SD and HF patients. Mean myocyte diameter and % area of disarray showed no differences among the 4 death groups. However, compared with NC, the other 3 groups, especially HF, had larger % area of massive fibrosis. The % area of massive fibrosis was correlated with LVDd (r=0.80, p<0.005), %FS (r=-0.64, p<0.05), and nRFR (r=-0.95, p<0.001) at the last evaluation. These results suggested that echocardiographic follow-up was useful in predicting the progression of the myocardial lesion and the prognosis of HCM.

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To clarify the prognostic significance of electrocardiographic changes in hypertrophic cardiomyopathy, we retrospectively evaluated serial electro-cardiograms in 77 patients with hypertrophic cardiomyopathy who were followed for more than 1 year. The electrocardiographic features analyzed were conduction disturbance and left precordial QRS voltage. There were 4 sudden deaths. Various conduction disturbances appeared in 32 (44%) of the remaining 73 patients. Intraventricular conduction delay was the most common (47%). The left precordial voltage decreased in 19 (26%), increased in 3, and did not change in 51. The left ventricular end-diastolic pressure at the initial investigation was significantly higher and clinical deterioration was more frequently seen in patients with a conduction disturbance or reductions increased significantly (from 4.4±0.6 to 4.8±0.7 cm in end-diastole and from 2.6±0.6 to 3.1±0.8 cm in end-systole; p<0.01, respectively) and left ventricular fractional shortening was reduced (from 41±8 to 36±11%; p<0.01) in the 32 patients with conduction disturbance during the follow-up period although absolute cavity size remained normal in 26 of these patients. These parameters did not change in those without conduction disturbance. Histopathological analysis of endomyocardial biopsies showed that myocardial fibrosis in the left ventricle was frequently associated with these electrocardiographic changes. However, such changes were not present in the sudden death patients. It is concluded that conduction disturbance and the reduction of QRS voltage are significant parameters which suggest a poor prognosis in patients with hypertrophic cardiomyopathy, but are not predictors of sudden death.

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Effects of cardiac pacing on secretion of atrial natriuretic polypeptide (ANP) were examined in 20 patients during cardiac catheterization under control conditions. The plasma ANP concentration in the coronary sinus (900±115 pg/ml) was significantly higher than those in the aorta (147±19 pg/ml) and the femoral vein (105±15 pg/ml) (p<0.001). The plasma ANP concentration was also significantly higher in the aorta than in the femoral vein (p<0.001). Its concentration at all three sites significantly increased during cardiac pacing (from 900±115 to 1461±218, from 147±19 to 250±36, and from 105±15 to 150±24 pg/ml, respectively). However, mean right atrial pressure and mean pulmonary capillary wedge pressure showed no significant changes between control conditions and during pacing (5±1 vs 6±1, and 8±1 vs 8±1 mmHg). Furthermore, there was no significant correlation between ANP secretion and the pressure in both atria. Thus, cardiac pacing can release ANP from the heart without increasing atrial pressure.

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To characterize the time dependence of prognostic markers for arrhythmia recurrence and arrhythmic death, 81 consecutive patients with documented sustained ventricular tachycardia (VT) or fibrillation (VF) and coronary artery disease (CAD) were analyzed. During follow-up, 28 patients had arrhythmia recurrence and 15 patients had sudden or arrhythmia death. Three different hazard phases were identified by fitting piece-wise exponential function curves to the distribution of both arrhythmia recurrence and sudden/arrhythmic death. An initial phase (0 to 6 months) had an arrhythmia recurrence rate of 2.1% per month; a second low-risk phase (6 to 38 months) had a rate of 0.88%; and a late high-risk phase (>38 months) had a rate of 2.2%. Sudden/arrhythmic death rates in each phase were 1.1%, 0.41%, and 1.7% per month, respectively. Separate Cox regression analyses within each phase identified the following independent predictors of arrhythmia recurrence: in the early phase, ejection fraction (EF) (p=0.033) and VT inducibility rank (p=0.048); and in the late phase, VT inducibility rank only (p=0.003). Likewise, independent predictors of sudden/arrhythmic death were: in the early phase, EF (p=0.049); and in the late phase, VT inducibility rank (p=0.008) and previous history of congestive heart failure (p=0.032). In CAD patients with documented sustained VT/VF, the probabilities of arrhythmia recurrence and sudden/arrhythmia death each followed a similar triphasic hazard function. Highest risk occurred in the late phase and the VT inducibility rank was predictive of late phase events, while EF was a predictor of early phase events.

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The concept of high lateral myocardial infarction (HLMI) has not been clearly defined, so criteria for its vectorcardiographic (VCG) diagnosis have had no firm basis. However, we have reported that HLMI, expressed as abnormal Q waves in lead aVL on the electrocardiogram, corresponds to necrosis of the area usually supplied by the diagonal branches of the left anterior descending coronary artery. Here, we evaluated conventional VCG criteria for the diagnosis of HLMI on the basis of angiographic findings, and selected the criteria of Chou as typical. The frontal plane VCG was analyzed in 46 and 194 patients with left ventricular hypertrophy. Chou's criteria had good specificity, but sensitivity was unsatisfactory (32/46, or 79%). Accordingly, we examined various parameters of the QRS and T loops and found that the addition of four new criteria to Chou's improved sensitivity (46/46, or 100%) without impairment of specificity. The additional criteria are; 1) initial counterclockwise rotation of the QRS loop, 2) the ration of the maximal QRS magnitude to the maximal T magnitude less than 4.5, 3) direction of the maximal T between +60° and +180°, 4) the QRS-T angle between 40° and 135°, all in the frontal plane.

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The attempted suicide by 2 women with a kyushin overdose is reported. Kyushin caused them to produce a significant elevation of a serum digoxin-like immunoreactive substance (2.35 and 1.84 ng/ml) and symptoms of nausea, vomiting and general malaise. Their blood biochemistry and electrolytes were normal. In one patient, and electrocardiogram revealed a second degree Wenckebach atrioventricular block and T-wave change. Toad venom, a kyushin ingredient, is possibly responsible for the development of these clinical features and electrocardiographic changes.

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At first, in order to know the causes of reperfusion injury, we studied myocardial injury by reperfusion in comparison with by Ca overloading, and the salvage of the myocardium from reperfusion and from CA overloading by Ca antagonist, diltiazem (DIL), in 52 anesthetized open-chest dogs. In myocardial mitochondria (Mit), Ca content was increased and Mg content and oxidative phosphorylation (State III) were decreased both by 120 min reperfusion after 60 min occlusion and by Ca overloading. Ca and Mg contents and oxidative phosphorylation of Mit were similarly changed by reperfusion as by Ca overloading. Electron-microscopically, myocardial injury by Ca overloading resembled reperfusion injury. Therefore, Ca inflow to myocardial cells may be one of the determinant factors which induce reperfusion injury. Although myofibrils were disorganized and contraction band necrosis appeared in these two types of myocardial injury, amorphous densities and glanular densities which indicated the irreversible injury of Mit appeared only in reperfusion injury. Then, the myocardial injury be Ca overloading is suspected of being mainly composed of the injury of myofibrils. The myocardial injury be reperfusion and by Ca overloading was prevented by DIL. These facts suggest that DIL may suppress Ca inflow and Mg outflow to myocardial cells. Second, to know the effect of positive isotropic agents on pump failure in acute myocardial infarction, we studied the effect of dobutamine (DOB) on the ischemic myocardium and the salvage of the ischemic myocardium from DOB-induced injury by DIL in 39 anesthetized open-chest dogs. After occlusion, the regional mechanical function of the acute ischemic myocardium was rapidly lost and % systolic shortening was negative level. In this situation, myocardial P_CO2 quickly increased and myocardial pH rapidly decreased. These parameters reached peak level after 20 min occlusion. Then, paradoxical improvement phenomenon appeared so that P_CO2 decreased and pH increased after that. Myocardial blood flow measured by thermocouples was stable at almost 10% of the preoccluded level for 1 90 min occlusion. These data suggest that anaerobic metabolism and residual aerobic metabolism can not supply the ischemic myocardium with enough energy and that irreversible injury may appear in the ischemic myocardium. As myocardial pH was shown as a mirror-image of P_CO2, the mechanism of CO₂ and proton production in the ischemic myocardium may be closely related. When DOB was administered after 40 min occlusion, P_CO2 increased and pH decreased again. Namely, the metabolic rate of these parameters rose again. But regional mechanical function was not recovered. When DIL was pretreated, P_CO2 and pH were not significantly changed by DOB administration from 40 min after occlusion. Therefore, DOB may not always improve the cardiac function of the ischemic myocardium and may cause the ischemic myocardial injury to deteriorate. It is possible that DIL will delay the progression of ischemic myocardial injury due to DOB.

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To define whether recanalization after occlusion can reduce the myocardial infarct size, we compared the infarct size in 25 pig hearts without collateral circulation, 35 dog hearts with collateral circulation and 11 human autopsied hearts with coronary thrombolysis at 2 to 6 hours after the onset of acute myocardial infarction. The data showed that % infarct size in the risk area increased according to the duration of occlusion. In the pig, % infarct size was 80±9% in the recanalization after 1 hour occlusion and 96±2% in the recanalization and the permanent occlusion group (95±3%). In the dog, % infarct size was 35±31% in the recanalization after 4 hour occlusion and 59±27% in the permanent occlusion group. In human autopsied hearts, the infarct size was was the same between the recanalization group (82±6%) and the permanent occlusion group (80±11%). The % infarct size in the recanalization groups was less than or the same as that in the hearts with permanent occlusion in dog, pig and human. Thus, it is concluded that, to reduce conclusively the infarct size, recanalization should be done within 1 hour after the occlusion in the hearts without collateral circulation and within 4 hours in the hearts with collateral circulation. So called reperfusion injury which means the greater expansion of the % infarct size than that in the permanent occlusion is not present.

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Pharmacological protection of acute ischemic myocardial injury was studied using diltiazem, bunazosin, coenzyme-Q₁₀ (Co-Q), and nicorandil, in dogs of which the left anterior descending coronary artery was ligated for 60 min. Drugs were given intravenously prior to and/or during coronary ligation. Co-Q, bunazosin and diltiazem suppressed degradation of sarcoplasmic reticulum (SR) expressed as inhibitions of reduction in Ca⁺⁺-dependent ATPase activity and degradation of major ATPase protein. Fine structures of ischemic myocardial cells were simultaneously retained as well. On the contrary, the effects of nicorandil on ischemic myocardial injury were few. It is likely that protection of ischemic myocardial injury could be expected with drugs which react with ischemic myocardium directly and inhibit excess inflow of extracellular Ca⁺⁺ in ischemic myocardium.

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The time course of recovery of left ventricular wall motion after coronary reperfusion and how that relates to anatomical infarct size, wall motion abnormality, and the amount of cardiac myosin light chain II release were evaluated in conscious dogs. One week after the implantation of hydraulic occluders on the left circumflex arteries, myocardial infarction was induced. Coronary reperfusion was performed 3 h after the occlusion in 9 dogs (R) and occlusion was sustained in 9 dogs (C). All dogs underwent serial 2-dimensional echocardiograms and determination of serum cardiac myosin light chain II. The infarct size was identified at 14 days. Systolic wall thickening at the center of the ischemic area (SWT) at 3 h was -7.7±2.8% (C), -9.9±3.0% (R). Systolic thinning was observed even at 14 days in C. Significant recovery of contraction was observed in R, but the improvement continued for as long as 2 days. SWT at 14 days was -1.5±2.8% (C) and 7.0±4.6% (R) (p<0.05). All of SWT or the extent of systolic thinning (EST) 3-hour and 14-day were correlated well with infarct size in C. In group R, 14-day SWT and 14-day EST correlated with infarct size but 3-hour SWT and 3-hour EST did not. Total release of serum cardiac myosin light chain II levels correlated well with infarct size (r=0.88), 14-day SWT (r=-0.90) and 14-day EST (r=0.89) in all dogs. These results indicate that both serum myosin light chain levels and the 2-dimensional echocardiography are noninvasive but quantitative techniques for evaluating infarct size after reperfusion. However, because of the presence of stunned myocardium, the magnitude of myocardial contraction abnormality early after reperfusion does not reflect ultimate infarct size.

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Pharmacological protection of acute ischemic myocardial injury was studied using diltiazem, bunazosin, coenzyme-Q₁₀ (Co-Q), and nicorandil, in dogs of which the left anterior descending coronary artery was ligated for 60 min. Drugs were given intravenously prior to and/or during coronary ligation. Co-Q, bunazosin and diltiazem suppressed degradation of sarcoplasmic reticulum (SR) expressed as inhibitions of reduction in Ca⁺⁺-dependent ATPase activity and degradation of major ATPase protein. Fine structures of ischemic myocardial cells were simultaneously retained as well. On the contrary, the effects of nicorandil on ischemic myocardial injury were few. It is likely that protection of ischemic myocardial injury could be expected with drugs which react with ischemic myocardium directly and inhibit excess inflow of extracellular Ca⁺⁺ in ischemic myocardium.

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We studied the effects of a thromboxane A₂ synthetase inhibitor (RS-5186), a thromboxane A₂ antagonist (ONO-3708), a 5-lipoxygenase inhibitor (AA-861) and a peptidoleukotriene antagonist (ONO-1078) on infarct size, polymorphonuclear leukocyte infiltration, gross myocardial hemorrhage and arrhythmias in the canine coronary occlusion (2 hour)-reperfusion model (5 hour). The infarct size and risk area were determined by a double staining technique. Thirty minutes prior to occluding the coronary arteries, dogs were randomly assigned to one of the following five groups: the thromboxane A₂ synthetase inhibitor group (n=11) receiving RS-5186 10 mg/kg i.v., the thromboxane A₂ antagonist group(n=12) receiving continuous intravenous infusion of ONO-3708 1 μg/kg/min, the lipoxygenase inhibitor group (n=11) receiving AA-861 3 mg/kg i.v., the peptidoleukotriene antagonist group (n=11) receiving continuous intravenous infusion of ONO-1078 1μg/kg/min and the vehicle control group (n=15). Except for ONO-3708, all the other drugs reduced the infarct size (RS-5186: 26.3±2.4% of risk area (mean±SEM), AA-861: 21.8±1.3%, ONO-1078: 22.5±4.4% vs control: 54.0±6.4%, p<0.01 respectively) as well as reducing the area of gross myocardial hemorrhage (RS-5186: 3.9±2.6% of infarct size, AA-861: 5.1±2.4%, ONO-1078: 5.2±2.5% vs control: 22.3±3.9%, p<0.01 respectively). RS-5186 and AA-861 reduced the intensity of polymorphonuclear leukocyte infiltration into the infarcted area, however, neither ONO-3708 nor ONO-1078 had any significant influence. These results suggested that eicosanoid products, especially thromboxane A₂ and leukotriene C₄, D₄ play important roles in the pathogenesis of myocardial ischemic and reperfusion injuries and that the new thromboxane A₂ synthetase inhibitor RS-5186, the lipoxygenase inhibitor AA-861, and the peptidoleukotriene antagonist ONO-1078 might be useful in salvaging ischemic myocardium.

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It has been suggested recently that oxygen-derived free radicals may play an important role in the genesis of reperfusion injury and arrhythmias. Free radicals have a very short half-life (ranging from mili- to microseconds), hence almost all the reports supporting the free radical hypothesis of reperfusion cell injury have been indirect. We have applied electrone spin resonance spectrometry to measure directly the amount of free radicals generated during ischemia and reperfusion. The concentration of free radicals in mitochondria increased significantly during ischemia (for 20 and 40 min). The concentration of free radicals after reperfusion was higher than that during ischemia, and a large amount of free radical generation occurred within the first 60 sec of reperfusion and returned to the level of prereperfusion at 5 min after reperfusion. The concentration of free radicals in the reperfusion-induced ventricular fibrillation group was significantly higher than that in the non-occurrence group. The administration of liposomal super-oxide dismutase reduced the incidence of reperfusion-induced ventricular fibrillation and that prevented the free radical generation during reperfusion. This study showed that enhanced generation of free radicals occurred at the onset of ventricular fibrillation and that free radical scavenger prevented the development of arrhythmias and free radical generation during reperfusion. We have obtained more circumstantial evidence for an involvement of free radicals in the genesis of reperfusion injury and arrhythmias.

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It has been proposed that a major target organelles damaged by the ischemic process, probably by the oxygen free radicals generated, is the portion of the excitation-contraction coupling system that regulates Ca²⁺ delivery (the sarcoplasmic reticulum and sarcolemma) to the contractile proteins. We tested this hypothesis by studying the effect of in vitro generation of oxygen free radicals from xanthine-xanthine oxidase system or dihydroxyfumarate (DHF)/Fe³⁺-ADP system on Ca²⁺ flux behavior of canine cardiac sarcoplasmic reticulum (SR); sarcolemmal (Na⁺, K⁺)-ATPase activity. Generation of oxygen free radicals by xanthine oxidase acting on xanthine as a substrate increased the passive Ca²⁺ effiux and decreased intravesicular Ca²⁺ with no effect on active Ca²⁺ influx (Ca²⁺-ATPase of SR vesicles. Similar exposure of sarcolemmal vesicles to xanthine plus xanthine oxidase stimulated Na⁺-Ca²⁺ exchange activity. When sarcolemmal vesicles were incubated with DHF plus Fe³⁺-ADP, (Na⁺, K⁺)-ATPase activity was decreased. It is postulated that the SR Ca²⁺ efflux pathways but not catalytic activity of the Ca²⁺ pump and sarcolemmal (Na⁺, K⁺)-ATPase involving Na⁺-Ca²⁺ exchange activity are altered by oxygen free radicals, and such changes may partly account for the occurrence of intracellular Ca²⁺ overload during the course of myocardial ischemia. Interestingly, oxygen free radicals from xanthine-xanthine oxidase system had no effect on myofibrillar pCa-ATPase curve. From this set of observations we would hypothesize that the SR and sarcolemma may be the principal target organelles of oxygen free radicals attack in the ischemic injury and not the contractile proteins per se.

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The Langendorff perfused rat heart was used to investigate whether myocardial damage during ischemia and reperfusion could be protected by free radical scavengers, calcium antagonist and adenosine. Myocardial high energy phosphates were measured by phosphorus-31 NMR spectroscopy during normal perfusion, 20 min of ischemia and 20 min of reperfusion. In hearts, which were treated both with free radical scavengers (FRS) (Superoxide dismutase): 24 IU/ml and catalase 22 IU/ml) and verapamil (10^-7 M), beta-ATP was significantly higher than that of FRS at the end of ischemia. However, beta-ATP recovered only to 83% of baseline value at the end or reperfusion. In view of myocardial metabolism, verapamil treated hearts were good for recovery of creatine phosphate (PCr) but not ATP at the end of reperfusion. Hearts which were treated with only adenosine did not differ from control hearts. However, when hearts were treated with both verapamil and adenosine (10^-4 M), recovery of both ATP and PCr content was significantly greater than that of control hearts. These results suggested that pretreatment with both verapamil and adenosine before and after global ischemia could protect ischemic myocardium, but, further studies are necessary to clarify the precise mechanism of protection.

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The purposes of this study were to investigate the sequential changes of PMN elastase during evolving myocardial infarction, and also to ascertain whether or not ulinastatin (UL), a clinically useful protease inhibitor, would affect the extent of ischemic myocardial injury. The levels of plasma PMN elastase (as α₁-proteinase inhibitor-elastase complex) were measured once in 13 normal controls, and at intervals in 30 acute myocardial infarction (AMI)patients given UL and 30 AMI controls on conventional therapy, and compared between the groups. The levels in control group on conventional therapy were significantly higher from 6 to 72 hours after the onset than those in normal controls. Maximum PMN elastase levels in non-survivors (n=7) were significantly higher than in survivors (n=23) at the 6-month follow-up (288.4±75.8 vs. 188.1±56.9μg/1, p<0.01). The maximum level of PMN elastase in patients given UL was significantly lower than that in the control group (162.2±96.2 vs 207.3±70.1μg/1, p<0.05), and the peak CK-MB in patients given UL was significantly lower than that in controls (252.3±150.9 vs 360.1±239.6 IU/1, p<0.05). Early mortality (seen at 6-month follow-up) in patients administered UL was significantly lower than that of the treated control (3.3% vs 23.3%, p<0.05). Analysis of changes in PMN elastase levels suggested that UL would be clinically beneficial for reduction of ischemic myocardial injury.

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Previous experimental studies have clarified the effectiveness of intermittent coronary sinus occlusion or ICSO. We evaluated the clinical feasibility, safety and effectiveness of ICSO in the patients with acute myocardial infarction (AMI) who were treated with concomitant thrombolytic therapy. Implementation of ICSO was obtained in 76% of the eligible patients. Twelve patients with evolving anteroseptal infarction treated with ICSO+thrombolysis were compared with 12 patients with anterior AMI treated with thrombolysis alone. Baseline characteristics were comparable between the two groups. Adverse effects of ICSO on hemodynamics, hemotalogic parameters and ventricular arrhythmias were not detected. Enzymatic infarct size, myocardial lactate metabolism in the acute phase, and left ventricular wall motion and T1-201 perfusion defect at follow-up in ICSO group were slightly improved compared with controls.

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In order to understand the mechanism of development asymmetric septal hypertrophy (ASH) in hypertension, 290 patients with essential hypertension (HT) were examined echocardiographically. Out of them 84 cases of advanced left ventricular hypertrophy (LVH) [37 cases of symmetric hypertrophy (HT-SH group) and 47 cases of ASH (HT-ASH group)] were compared in their clinical and echocardiographic findings with hypertrophic cardiomyopathy (HCM). In the 290 HT cases, the highest systolic pressure in each patient's history was found to correlate with left ventricular (LV) posterior wall thickness (PWT), but not with the septal wall thickness (IVST). There were no differences in LV thickness (IVST+PWT) among patients in the HT-ASH, HT-SH and HCM groups. While the HCM group patients showed no significant differences in IVST and PWT from those in the HT-ASH group, they did have greater IVST and smaller PWT than HT-SH group patients. The rapid filling rate (RFR) was also not much different in the HCM and HT-ASH groups, but was significantly lower in the HCM group than in the HT-SH group. Furthermore, HT-ASH group patients has a milder degree of hypertension and a higher incidence of familial occurrence of HCM than did those in the HT-SH group. After treatment for HT, the HT-SH group showed a significant decrease in wall thickness during long-term observation, while the HT-ASH and HCM groups, failed to exhibit such changes. Moreover, the degree of myocardial disarrangement in the HT-ASH group did not differ significantly from that in the HCM group. These results suggested that LVH in HT is related not only to pressure load but also to genetic factors similar to that in HCM.

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