Wall stress has been used as one of the parameters of myocardial mechanics. The present review focuses on recently developed data on ventricular wall stress, especially in relation to other newly developed areas in cardiology. In hypertensive hearts, there is a broad continuous spectrum in the structural and functional changes: those with low wall stress (inappropriate hypertrophy), those with normal wall stress (appropriate hypertrophy) and those with high wall stress (inadequate hypertrophy). Among them, the responses to neurohumoral stimuli are various, and their clinical features and courses also varied. These differences in wall stress among the different categories of hypertensive hearts may be caused by the variable influences of non-mechanical factors, such as molecular, metabolic and neurohumoral ones. Wall stress is an essential determinant of myocardial oxygen consumption, and is also an important determinant of the myocardial contractile state and diastolic function. In contrast to excitation-contraction coupling, contraction-excitation feedback has been studied, suggesting the importance of wall stress regulating electrical phenomena. The interrelationship between mechanical factors (including wall stress) and non-mechanical factors (including molecular, metabolic, neurohumoral and genetic ones) has been investigated intensively. In conclusion, wall stress (or force on the myocardial cell) may be a keystone in cardiology, relating to each of the cardiac phenomena. If wall stress deviates from the normal range, even with compensatory mechanisms, severe cardiac events occur. The compensatory mechanisms for wall stress may act as a risk factor on the heart, especially when the wall stress remains outside the normal range.

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Although limited numbers of elderly subjects have occasionally been included in population-based studies, only a few studies have been conducted specifically on elderly hypertensives, and practically none at a population level.We studied 655 hypertensive subjects from a cohort of 2, 254 elderly subjects. The intervention consisted of the creation of a Hypertension Outpatients' Clinic under our auspices but with complete co-operation from general practitioners, randomizing the identified hypertensive patients into pre-established therapeutic drug regimens, and early follow-up recording of mortality for 7 years. The drugs used were clonidine (n=61), nifedipine (n=146) and the fixed combination of atenolol+chlorthalidone (n=144); 304 subjects underwent "free therapy" by their personal physicians without any special intervention. There were 1, 404 normotensive subjects.Overall 7-year follow-up mortality was 34.9% in the hypertensive subjects receiving "free therapy", 22.5% in those receiving "special care", and 24.2% in the normotensives. Cardiovascular mortality was respectively 23.7%, 12.2%, and 12.0%. Overall and cardiovascular annual cumulative mortality were significantly lower in the "special therapy" than in the "free therapy" group. The fixed combination of atenolol and chlorthalidone reduced mortality below that of the normotensives, independent of other cardiovascular risk factors.

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One hundred and thirty-five patients with malignant hypertension seen over a period of 11 years (1979 to 1989) at a referral hospital were analyzed to characterize the clinical features and etiology of this disease. Ninety male and 45 female patients with an average age of 38.2±1.4 years were studied. Malignant hypertension was the presenting feature in 68 patients. The etiology included essential hypertension in 88 patients and a secondary cause in 47 patients. Secondary causes included a renovascular etiology in 20 patients, renal parenchymal disease in 19, pheochromocytoma in 6 and Conn's syndrome and adrenal carcinoma in one patient each. Among the 20 patients with renovascular hypertension, Takayasu's arteritis was seen in 15 (75%). The mean age of patients with essential hypertension was 41.7+1.14 years while the mean age in patients with secondary hypertension was 33.2+1.96 years. Duration of pre-existing hypertension was longer in essential hypertensives (2.42+0.45 years) than in patients with secondary hypertension (1.27+0.41 years, ρ<0.05). Raised serum creatinine was seen in 93 patients. Seventy-seven patients had left ventricular hypertrophy on ECG. Ninety-six patients were followed for a period ranging from 18 months to 10 years (mean 32 months). Sixteen patients died during hospital stay while 6 patients died during the follow-up period. The deaths were related to the effects of uncontrolled hypertension including, renal failure (11), stroke (6), congestive cardiac failure (3) and myocardial infarction (1). Male sex, higher age at presentation and deranged renal function at presentation were associated with a poor outcome. Thus, essential hypertension is the most common cause of malignant hypertension in India. Takayasu's arteritis is the most common cause of secondary hypertension. Impaired renal function and poor compliance affect the prognosis of malignant hypertension adversely.

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With rapid ventricular pacing, sustained ventricular tachycardia (VT) is often entrained and interrupted at a critical paced cycle length. In this paper, the possible mechanism and determinant of the critical cycle length interrupting VT are addressed.
Sixteen consecutive patients underwent rapid ventricular pacing in 18 morphologically distinct sustained VTs before and after procainamide. The VT morphology was identical before and after the drug.
The VT origin was determined by endocardial mapping as the earliest site of activation of VT and an electrode catheter was located at the site. Rapid pacing was performed to entrain VT and repeated in 10msec decrements of cycle length until VT was interrupted at a critical paced cycle length which was defined as the block cycle length.
The effective refractory period was measured at the pacing site. The paced QRS duration and the local conduction time were measured and used as indices of conduction time in the normal myocardium.
VT was entrained and interrupted in all patients. At the block cycle length, initial constant fusion was replaced abruptly by the fully paced QRS complex. At the same time, the local electrogram at the site of VT origin showed changes in the morphology and the timing of activation which were identical to those of the fully paced beat. This loss of fusion and the changes in the local electrogram were considered to be a result of orthodromic block and the block cycle length was assumed to represent the cycle length at which 1:1 conduction fails in the area of slow conduction.
After procainamide, both the VT cycle length and the block cycle length were prolonged to a similar degree (p<0.001) but the relative degree of change varied from patient to patient.
The paced QRS duration and the conduction time were prolonged by procainamide but in smaller degrees than the cycle length of VT or the block cycle length (p<0.02-01). The effective refractory period at the pacing site and the QT interval showed small changes after procainamide.
The postrepolarization refractoriness rather than the duration of action potential can be responsible for the procainamide-induced prolongation of the block cycle length, and the block cycle length might be used as a new index to characterize the electrophysiologic property of the VT circuit and also the action of antiarrhythmic drugs.

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Atrial demand pacing provides a physiological, simply implemented, and less costly alternative of cardiac stimulation in symptomatic sick sinus syndrome (SSS) patients. Hindrance from widespread use stems mainly from the potential development of high degree AV block and persistent atrial fibrillation. A reappraisal of atrial pacing is now justified as we gain more clinical information. In this study we examined retrospectively the clinical course of 22 well-selected SSS patients paced in AAI mode for 30±29 months. Two patients had infrequent short-run atrial tachyrhythmia before implantation. There was an early lead dislodgement which required repositioning later. Three acute threshold increments were noted which necessitated a change in atrial pacing site in one and short-term steroid use in the other two. No other sensing, pacing or operative complication occurred and all pacing systems performed well. All patients survived during follow-up and no patient developed congestive heart failure, though depressed left ventricular function was found in three preoperatively. No high degree AV block was encountered. Four patients presented paroxysmal atrial fibrillation (PAF) 25±16 months after the procedure, of whom one developed chronic atrial fibrillation. No single factor predicted the development of PAF. Resumption of normal pacemaker function always occurred immediately in the pause following cessation of PAF and no revision of pacing mode was required in the patient with chronic AF. Symptomatic relief was obtained in all patients. In summary, single chamber, single rate atrial pacing remains a physiologic, reliable, economic and easily implemented pacing modality affordable to a number of sick sinus patients. Maintenance of atrial pacing is feasible in the presence of paroxysmal/chronic atrial fibrillation.

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This study was planned to determine the presence and extent of cardiac involvement in metabolic storage diseases, including types I and II glycogenoses, Gaucher and Neimann-Pick diseases, galactosialidosis and mucopolysac-charidosis. M-mode, 2-dimensional and Doppler echocardiographic studies were used for the determination of left ventricular wall thickness, systolic function, anatomic derangement, valvular dysfunction and left ventricular diastolic function in the patient and control groups. In 19.35% of the cases valvular involvement, and in 59.26% thickening of the left ventricular wall due to metabolic storage, was found. Left ventricular systolic function was in the normal range. The diastolic mitral flow patterns of the cases showed obstructive type changes.
It can be concluded that in this study, besides previously described cardiovascular changes, some new findings have been detected by means of echocardiography in patients with metabolic storage diseases.

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We used an anesthetized swine model of regionally "stunned" myocardium to determine the effect of stunning on coronary autoregulation and blood flow heterogeneity. In 18 domestic swine, stunning was accomplished by reducing blood flow to the left anterior descending coronary artery (LAD) by approximately 75% of baseline for 15min and restoring it to normal for 1 hour. We quantified coronary autoregulation using both the slope of coronary pressure-flow curves and an autoregulation index. We quantified blood flow heterogeneity using radioactive microspheres to determine the variability in flow (dispersion index) among forty 200mg segments of myocardium from the center of the stunned, LAD-perfused left ventricle. Before and after stunning, we measured autoregulation, myocardial blood flow and flow heterogeneity, as well as hemodynamic indices of myocardial oxygen demand. Fifteen min of ischemia and 1 hour of reperfusion produced both a 46% reduction in mechanical function, and a 7% drop in systemic arterial pressure, but no change in heart rate or rate pressure product. Myocardial oxygen consumption was 15% reduced and myocardial blood flow 16% reduced in the stunned myocardium when measured at one hour of reperfusion. Fifteen min after reperfusion, the slope of the coronary pressure flow plots and the coronary venous oxygenation were increased whereas the autoregulation index decreased. These findings all indicate reduced autoregulation during early reperfusion. However, after one hour of reperfusion, the slope of the coronary pressure-flow relation (0.41±0.19 vs. 0.48±0.26ml•100g^-1•min^-1•mmHg^-1) and the autoregulation index (0.43±0.16 vs. 0.30±0.32) were unchanged from control measurements (p>0.05). Blood flow heterogeneity remained normal in the stunned myocardium. These findings challenge the hypothesis that the mechanical dysfunction of the stunned myocardium is due to suboptimal perfusion resulting from poor coronary autoregulation or maldistribution of blood flow.

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The hyperresponsiveness of cardiac tissue to histamine following treatment with reserpine was pharmacologically characterized. Guinea pig hearts were isolated 24 hours after intraperitoneal administration of 5mg/kg reserpine. This treatment resulted in a complete depletion of tissue norepinephrine. Reserpine treatment potentiated the positive inotropic response of isolated perfused hearts to histamine at doses ranging from 0.3 to 3μg (23 to 57% increase for reserpine-treated animals vs. 14 to 32% increase for control animals). Isolated left ventricular papillary muscle of reserpine-treated guinea pig hearts also showed hyperresponsiveness to histamine at concentrations of 0.1μM or greater. The hyperresponsiveness of the papillary muscle contraction of the reserpine-treated animals to histamine was abolished in the presence of 1μM cimetidine, but not attenuated in the presence of 1μM diphenhydramine. This hyperresponsiveness was not modified by 1μM bunazosin or 1μM propranolol. The results suggest that H2-receptor mediated action plays a role in the hyperresponsiveness of cardiac muscles to histamine.

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We measured [Ca²⁺]i of guinea pig and rat myocytes with Ca²⁺ waves, using fura-2 fluorescence image processing. In guinea pig myocytes, Ca²⁺ waves were absent during the control perfusion period, but could be induced by the addition of strophanthidin (100μM) or sodium cyanide (NaCN: 2mM) to the perfusate. The [Ca²⁺]i increased from the control values of 69±5nM and 46±2nM, to 263±9 (p<0.05 vs. control) nM and 225±20 (p<0.05) nM, respectively, when cells exhibited Ca²⁺ waves. Although 13% (16 of 121) of the rat myocytes displayed Ca²⁺ waves during the control perfusion, the [Ca²⁺]i with Ca²⁺ waves (56±9nM) did not differ from [Ca²⁺]i in the absence of Ca²⁺ waves (54±3nM). Ca²⁺ waves were induced by the perfusion with a high Ca2+ solution (24.5μM) or NaCN (2μM), and [Ca²⁺]i increased from the control values of 67±11nM and 74±5nM, to 231±41 (p<0.05 vs. control) nM and 266±64nM, respectively, when cells exhibited Ca²⁺ waves. The Ca²⁺ waves were abolished by the removal of extracellular Ca²⁺, or by the perfusion with ryanodine (10μM) or caffeine (20mM). In conclusion, it was shown that Ca²⁺ waves were due to oscillatory Ca²⁺ release and that the absolute value of [Ca²⁺]i is important for the appearance of Ca²⁺ waves in guinea pig and rat myocytes. However, some rat myocytes with a control [Ca²⁺]i level exhibited spontaneous Ca²⁺ waves during the control perfusion, showing a species difference in the susceptibility to oscillatory Ca²⁺ release from the sarcoplasmic reticulum.

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A 75-year-old female had syncopal episodes from Torsade des Pointes (TdP). Her electrocardiogram showed a prolonged QT interval which was not associated with electrolyte imbalances or drug therapy. Similar electrocardio-graphic abnormalities were found in three family members.
Electrophysiologic study showed a mildly prolonged effective refractory period of 260-290msec, but no tachyarrhythmia was induced. Coronary arteriography was normal but intracoronary acetylcholine unexpectedly induced a prolongation of the QT interval and TdP. Direct action of acetylcholine on the ventricular muscle was suggested.

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A 57-year-old male who had arrhythmogenic right ventricular dysplasia (ARVD) with recurrent atrial flutter (AF) is reported. The patient had more frequent episodes of AF than of ventricular arrhythmias. Magnetic resonance imaging, echocardiography and right ventriculography revealed dilatation of the right ventricle and endomyocardial biopsy specimens from the right ventricle showed findings which were compatible with ARVD. The left ventricular specimen, however, also revealed a loss of myocytes and interstitial fibroelastic changes. The present case demonstrates an overlap of post-inflammatory or primary endomyocardial fibroelastic changes with ARVD.

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In secondary amyloidosis (AA type), clinically significant cardiac and gastrointestinal involvement are uncommon, in contrast to the primary type. We report a case presenting with chronic diarrhea and cardiac manifestations who was diagnosed as having AA-amyloidosis with unknown predisposing illness based on endomyocardial, rectal and subcutaneous fat tissue biopsies.

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