Hemodynamic parameters during supine leg exercise-induced myocardial ischemia were investigated in ten patients without left ventricular hypertrophy (group I), and in ten patients with left ventricular hypertrophy (group II) . Both groups of patients had previously been diagnosed as having totally asymptomatic silent myocardial ischemia. Both groups were comparable in age, sex, left ventricular ejection fraction at rest, and extent of coronary artery disease. All of the patients exercised to the same extent without angina or its usual equivalent. Left ventricular filling pressure increased from 4±2 mmHg at rest to 11±3 mmHg at peak exercise in group I, and from 7±4 mmHg at rest to 19±7 mmHg at peak exercise in group II. Left ventricular filling pressure at peak exercise was significantly greater in group II than in group I (p<0.01). Totally asymptomatic silent myocardial ischemia can be seen with either normal or mildly abnormal left ventricular filling dynamics during exercise. In addition, patients with coexistent left ventricular hypertrophy can have severely abnormal left ventricular filling dynamics during exercise without ischemic cardiac pains. Therefore, severe ischemia and/or stretching of the ventricular wall may be necessary, but not sufficient, for the occurrence of chest pain.

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Our objective was to investigate the changes in renal hemodynamics, and the role of these changes in the pathogenesis of essential hypertension. We used a thermodilution renal vein catheter and measured left renal blood flow in 21 patients with essential hypertension. Arterial pressure was monitored concurrently. Cardiac output was measured in 11 patients to calculate total peripheral vascular resistance. Systolic, diastolic, and mean arterial pressure were 187±7 mmHg, 97±5 mmHg and 127±5 mmHg, respectively. Left renal blood flow was 8.01±0.38 ml/s. Left renal vascular resistance, calculated as mean arterial pressure divided by left renal blood flow, was 16.4±0.8 mmHg ml^-1s, and was positively correlated with systolic, diastolic and mean arterial pressures (p<0.05). However, no significant correlation was observed between arterial pressure and left renal blood flow. Plasma renin activity in left renal venous blood, measured in 15 patients, was not significantly correlated with renal hemodynamics. Cardiac output and total peripheral vascular resistance were 81.4±6.0 l/min and 1.68±0.18 mmHg ml^-1s, respectively. Total peripheral vascular resistance was not significantly correlated with either left renal blood flow or renal vascular resistance. The data suggest that a rise in renal vascular resistance may parallel the rise in blood pressure, but not that of total peripheral vascular resistance.

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The initiating mechanism of torsades de pointes is still unclear, although it is believed to be related to repolarization abnormalities such as QT prolongation and abnormal U wave. Recording monophasic action potentials in vivo can provide useful information about ventricular repolarization. To investigate the mechanism of torsades de pointes, monophasic action potentials were recorded by the contact electrode method in 20 patients. The patients were classified into three groups (Group 1 ; 4 patients at the acute phase of torsades de pointes, Group 2; 6 patients at the improved phase of torsades de pointes, Group 3; 10 patients with bradyarrhythmias without torsades de pointes). Action potential duration 90% (duration from monophasic action potential upstroke to 90% repolarization), repolarization time (duration from QRS onset to 90% repolarization), and effective refractory period were measured at several right ventricular endocardial sites during spontaneous rhythm and right ventricular pacing at several pacing cycle lengths. Humps during the repolarization phase were observed in all of the patients in Group 1 and in 1 patient in Group 3 during spontaneous rhythm. Action potential duration 90% and repolarization time in Group 1 were significantly longer than those in Groups 2 and 3. The dispersion of action potential duration 90% and repolarization time in Group 1 were also greater than those in Groups 2 and 3. With rapid ventricular pacing, the hump observed in Group 1 either disappeared completely or the amplitude of the hump decreased, and the dispersion of the action potential duration 90% and repolarization time was also reduced. A significant correlation was observed between action potential duration 90% and effective refractory period. (r=0.78, p<0.001) In conclusion, these results suggest that the hump and the dispersion of repolarization play a key role in the genesis of torsades de pointes. Pacing therapy may be useful in correcting these abnormalities.

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The purpose of this study was to investigate the relation between free radicals and the effect of preconditioning on reperfusion arrhythmias using the isolated working rat heart model. Rats were divided into 3 groups: control, preconditioned without superoxide dismutase (SOD) and preconditioned with SOD (n=8 each group). The incidence of reperfusion-induced ventricular fibrillation (Vf) in the preconditioned without SOD group was reduced from 100% to 13% (p<0.005 vs control). This protective effect of preconditioning was not observed in the SOD-treated group (incidence of Vf increased from 13% to 75%, p<0.025). The protective effect of preconditioning on reperfusion arrhythmias is related to the presence of oxygen free radicals which occur during the reperfusion period of the preconditioning phase.

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We evaluated the reliability of a new device for indirect measurement of systolic blood pressure in normal and hypertensive New Zealand White rabbits. This device consisted of an ear unit composed of an air chamber and sensitive photoelectric sensors, and was connected to an apparatus used for the tail-cuff method. Systolic blood pressure was determined by simultaneous recordings of pulse volume oscillations of the central ear artery and the chamber pressure. The blood pressure in 8 normal rabbits was 116±7/78±6 mmHg (mean ±SEM) by direct measurement and 100±6 mmHg by indirect measurement. In a one-kidney, one-clip hypertensive model, the new device showed that blood pressure increased from 100±7 to 158±7 mmHg over 4 weeks. After nicardipine was injected, blood pressure fell from 191±10/114±10 to 117±7/72±8 mmHg as measured by the direct method, and from 158±7 to 92±6 mmHg as measured by the new device. A strong correlation (r=0.91, p<0.01) was observed between direct and indirect measurements. Our findings indicate that this device provides rapid, easy and reliable measurement of blood pressure in rabbits.

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The effects of pre-existing collaterals (PC) and the perfusion size (PS) on the ischemia-induced collateral development were studied in a canine model. Under aseptic conditions, the dogs were instrumented with pairs of ultrasonic crystals to measure regional wall motion in the territory of the left circumflex (LCX) and left anterior descending coronary artery. A micromanometer was used to measure left ventricular (LV) pressure. Two to 3 weeks after surgery, 2 min coronary occlusion (CO) of LCX was repeated every 32 min consecutively day and night using a remote control, motor-driven hydraulic cuff occluder. Regional wall motion and LV pressure were monitored via a telemetry system in 23 dogs. The functional state of PC was estimated by the level of % reduction of regional wall motion at the end of the first 2 min CO, which ranged from -11 to -141%. PS of LCX area at risk determined by the post mortem angiograms ranged from 35 to 54% (mean ±SEM; 44±1%) of LV. Number of CO needed for collateral development ranged from 8 to 628, and was exponentially related to the functional state of PC (r=-0.77, n=23, p<0.01), but not to PS (r=0.43, n=19, p=0.07). These results suggest that the functional maturity of pre-existing collaterals is one of the major determinants of collateral development related to ischemic stimuli.

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Cold preservation of isolated mammalian hearts attenuates cardiac contractility. We examined the effect of intracellular and extracellular Ca ion on the contractility of cold-preserved atria of rat. Rat hearts were isolated and stored in Collins' solution at 4°C for either 0 or 12 h. Mechanical responses were then examined in electrically driven left and beating right atrial muscle preparations. When stimulus frequencies were increased stepwise from 0.1 to 3 Hz, the twitch contractions initially decreased (Woodworth phenomenon: WP) and then increased (Bowditch phenomenon: BP) in 0 hour-preserved (fresh) left atrial preparations. However, BP, but not WP, was abolished in 12 hour-preserved preparations. The absence of BP was also observed when fresh preparations were exposed to a low-Ca medium (0.9 mM) . Ryanodine (3×10^-8 M) abolished the twitch contractions at low stimulus frequencies, but did not inhibit BP in fresh preparations. In 12 hour-preserved preparations, both ryanodine and low-Ca medium completely inhibited the twitch contraction. The positive inotropic effects of isoproterenol in right and left atria were markedly attenuated after 12-hour cold preservation. However, the rate of spontaneous beating and the positive chronotropic effect of isoproterenol in right atria were not changed in the cold-preserved preparations or in fresh preparations that had been treated with ryanodine or exposed to a low-Ca medium. These results clearly show that cold-preserved atrial muscle is more susceptible to changes in intracellular and extracellular Ca ion and suggest that the attenuation of cardiac contractility by cold preservation may be due to the impairment of Ca²⁺ influx which may result from membrane deterioration.

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Creatine kinase (CK) isomers have recently been suggested to be of value in the diagnosis of acute myocardial infarction (AMI) . The aim of this report was to determine whether measurement of CK isomers, especially the MM isomer and the cardio-specific marker MB isomer, is practical in the diagnosis of AMI. A 64-year-old female with consistently high values for total CK showed an electrophoretic pattern which suggested AMI. We ruled out all possible causes of increased CK, and its MB isomer, including IgGBB, beta-LP (lipoprotein) and mitochondrial complexes as well as myocarditis, muscular disorders, and myoglobinuria. Regardless of the source of the anomaly, the fact remains that CK macroanomaly cases can be an obstacle in the diagnosis of AMI. CK isomers have proven to be accurate markers in AMI and valuable in doubtful cases, such as non Q-AMI. However, in light of this particular case of CK macroanomaly, isomers are not 100% accurate (specific) in the diagnosis of AMI.

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A 43-year-old male with history of recurrent episodes of syncope, non-sustained wide complex tachycardia and structurally normal heart was studied. Syncope was induced with upright tilt provocation, while monitoring cerebral blood flow velocity with Doppler ultrasound, concurrently with invasive blood pressure, heart rate and rhythm determination. Postural induced cerebral hypoperfusion preceded hypotension and cardiac asystole. Treatment with ephedrine and transdermal scopolamine was effective in preventing symptoms.

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We report a case of idiopathic pericarditis in a 71-year-old woman without a friction rub or electrocardiographic changes suggestive of pericardial inflammation. She noticed dyspnea and palpitation on exertion about 40 days before admission. After admission, pericardial effusion and inflammatory reactions, such as elevated C-reactive protein, were found. Moreover, gallium-67 citrate scintigraphy revealed abnormal isotope accumulation over the cardiac silhouette. Therefore, she was diagnosed as having "active" pericarditis. The finding with the gallium scan became negative with steroid therapy. In this case, a gallium scan was very useful in assessing and monitoring the course of pericardial inflammation.

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