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We report here the occurrence of pink sapphires in association with a variety of gemstones from the Trivandrum Granulite Block south of the Achankovil Shear Zone in southern India. The mineralization is associated with pegmatites or veins emplaced within granulite facies aluminous supracrustals. The sapphires show near-pure A1,0, composition (98.43-99.48 wt.%) with traces of Cr, O, (0.02-0.12 wt.%) and FeO (0.01-0.12 wt.%). The available radiometric age of 513-∼2 Ma for gem quality zircon associated with pink sapphire in the Melankode locality confirms that the mineralization is of late Pan-African age. Pink sapphires have been widely reported from a number of localities in southern Madagascar including Betroka, Illakaka, Antranondambo and Ambossary. Sapphires of various hues also occur in the Ratnapura gem district in the southwestern part of Sri Lanka. The pink sapphire occurrences in southern Madagascar and southern Kerala provide strong evidence for India-Madagascar juxtaposition in the Gondwana assembly with the Ranotsara Shear Zone in southern Madagascar extending into the Achankovil Shear Zone in southern India.

The administration of calcium antagonists to patients with healed myocardial infarction is a controversial treatment. This study was conducted to elucidate the effect of short-acting nifedipine and diltiazem on cardiac events in patients with healed myocardial infarction.A controlled clinical open trial of 1115 patients with healed myocardial infarction was carried out between 1986 and 1994. The patients included 595 who received no calcium antagonist, 341 who received short-acting nifedipine 30 mg/d, and 179 who received short-acting diltiazem 90 mg/d. The primary end points were cardiac events, which were defined as fatal or nonfatal recurrent myocardial infarction; death from congestive heart failure; sudden death; and hospitalization because of worsening angina, congestive heart failure, or premature ventricular contractions. Cardiac events occurred in 51 patients (8.6%) in the no-calcium-antagonist group and 54 (10.4%) in the calcium-antagonist group (odds ratio, 1.24; 95% CI, 0.83 to 1.85), demonstrating that the calcium antagonists did not reduce the incidence of cardiac events. Subgroup analysis revealed no beneficial effects of these drugs for reducing cardiac events in patients with such complications as hypertension or angina pectoris.This study showed that use of short-acting nifedipine and diltiazem in this postmyocardial infarction population was associated with a 24% higher cardiac event rate, but this strong adverse trend did not reach statistical significance.

The present study investigated whether the exercise-induced ST-segment elevation can predict the prognosis for patients with myocardial infarction. Among 529 patients with myocardial infarction, 411 underwent treadmill exercise testing about 5 weeks after the onset. All patients were followed up (mean [+/-SD] 54 +/- 41 months) to compare the incidence of cardiac events. One hundred and eighteen patients (22%) could not perform the exercise test due to cardiac or noncardiac limitation. Ineligibility for exercise test was most useful for risk stratification. Multivariate analysis showed that elimination from the stress test with cardiac limitation was the most significant predictor for cardiac death. Excluding the 16 patients with bundle branch block, the 395 patients were classified into four groups of ST-segment elevation (107 cases, 27%), ST-segment elevation combined with depression (22 cases, 6%), ST-segment depression (106 cases, 27%), ST-segment unchanged (160 cases, 40%). Among the various stress test abnormalities, only low exercise duration was a predictor for cardiac death. ST-depression and ST-elevation combined with depression were independent risk predictors for all cardiac events. Most patients with ST-elevation had single-vessel disease with excellent exercise capacity and low incidence of cardiac events. ST-segment elevation during exercise 5 weeks after myocardial infarction is not associated with a poor prognosis.

The efficacy of combining antiplatelet agents with low doses of aspirin to prevent cardiac events in patients with myocardial infarction was examined. A total of 1,083 patients with prior myocardial infarction were randomly divided into those who were (618) and were not (465) treated with antiplatelet agents, and observed for 12.5 +/- 18.5 months. Those treated with antiplatelet agents included 113 patients treated with aspirin (50 mg) plus dipyridamole (150 mg/day), 253 treated with aspirin (50 mg) plus ticlopidine (200 mg/day), and 252 treated with only 1 of the 3 antiplatelet agents. Cardiac events, including fatal or nonfatal recurrent myocardial infarction, death by congestive heart failure, and sudden death, occurred in 34 patients (7.3%) in the nontreatment group and in 19 patients (3.1%; p0.01) in the treatment group; odds ratio 0.40, 95% confidence interval 0.23-0.71. There were only 2 cardiac events (1.8%) in the aspirin + dipyridamole group (p0.05 vs nontreatment group: odds ratio 0.28: 0.08-1.03), and 5 such events (2.0%) in the aspirin + ticlopidine group (p0.01; odds ratio 0.28: 0.11-0.69). Subgroup analysis to exclude differences in the patients' background confirmed the efficacy of these antiplatelet agents. We conclude that combined treatment with low doses of aspirin plus either dipyridamole or ticlopidine is effective in preventing cardiac events in patients who have had prior myocardial infarction.

A 58-year-old man was involved in an automobile accident and suffered remittent fever, leukocytosis and high C-reactive protein level. He developed a diastolic murmur 2 months after the accident. Transesophageal echocardiography showed severe aortic regurgitation with a vegetation-like echo image attached to the right coronary cusp leaflet, suggesting infective endocarditis. Intensive medical treatment for 11 months did not improve the vegetation-like echo-image, so aortic valve replacement was performed. Disruption of the right coronary cusp leaflet was confirmed surgically. Prolapse had occurred as a result of disruption during diastole. The vegetation-like echo-image was considered to be the tip of this leaflet.

The prevention of left ventricular aneurysm formation and left ventricular remodeling by percutaneous transluminal coronary angioplasty (PTCA) performed 24 to 48 hours after onset of acute myocardial infarction was investigated. Left ventriculography and coronary angiography were performed in 25 patients within 24 hours of onset of acute myocardial infarction. The patients were divided into two groups; reperfusion group (n = 17) and successful PTCA group (n = 8). The reperfusion group and the PTCA group included patients whose infarct-related coronary arteries were successfully reperfused to 99%, Thrombolysis in Myocardial Infarction (TIMI) grade II or III, immediately after coronary thrombolysis. However, the reperfusion group did not include the patients with spontaneous reperfusion or reperfusion after PTCA. The PTCA group consisted of patients who underwent successful PTCA performed within 24 to 48 hours after onset of infarction (mean 28.4 +/- 6.0 hours). Non-reperfusion in the acute phase was defined as TIMI grade 0-I. The size of the ventricular aneurysm in the PTCA group was significantly reduced compared with the reperfusion group (PTCA group 4.2 +/- 8.7%, reperfusion group 27.2 +/- 6.6%; p0.01). The increase of left ventricular end-diastolic volume (delta LVEDVI) from the acute to chronic phases was calculated to estimate left ventricular remodeling. There was a significant difference between the two groups in delta LVEDVI (PTCA group 4 +/- 19 ml/m2, reperfusion group 19 +/- 17 ml/m2; p0.05). PTCA performed within 24 to 48 hours after onset in patients with acute myocardial infarction and infarct-related coronary arteries, resulting in reperfusion to 99% TIMI grade II or III immediately after coronary thrombolysis, prevents left ventricular aneurysm formation and remodeling.

Two-dimensional echocardiography was used for diagnosing coronary vasospasm during the cold pressor stress test immediately after hyperventilation in five patients with suspected vasospastic angina. The test consisted of hyperventilation for 6 min and cold water pressor for 2 min under continuous electrocardiographic and echocardiographic monitoring. Coronary angiography with intracoronary injection of acetylcholine was performed in all patients within 1 month after the stress test. During the stress test, new asynergies of both the anterior and inferior walls were seen in three of the five patients, and new asynergy of the anterior wall in the other two patients. All acetylcholine induced coronary artery spasms occurred at the same locations as the new asynergies provoked by the stress test. In three patients, wall motion abnormality occurred earlier than ST segment elevation, and the other two patients had no ST changes. Chest pain was induced in three patients and delayed in comparison to electrocardiographic and echocardiographic changes. Echocardiographic monitoring during the stress test could detect spasms unaccompanied by either ST segment changes or chest pain, and could detect multivessel coronary spasms. Hyperventilation and cold pressor stress echocardiography may be used for the diagnosis of vasospastic angina.

Dobutamine stress echocardiography was used in the diagnosis of myocardial ischemia in patients with implanted VVI pacemakers. A 69-year-old woman received a pacemaker for Mobitz II type AV block in October 1992. She had suffered from chest pain during effort since January 1993 and underwent dobutamine stress echocardiography in April 1993. Although the electrocardiogram failed to identify ischemia because of the pacemaker rhythm, ischemia of the anterior wall was revealed as a worsening of the wall motion on the echocardiogram. The coronary angiogram showed 99% stenosis of the left descending artery. A direct coronary atherectomy was performed on the lesion. A 68-year-old man received a pacemaker for sick sinus syndrome in August 1993. He had suffered from chest oppression during effort since May 1992 and underwent dobutamine stress echocardiography in October 1993. Spontaneous rhythm appeared with dobutamine infusion, but the electrocardiogram could not demonstrate ischemia because of incomparability with the rhythm at rest. Echocardiography detected a new wall motion abnormality of the inferior wall caused by dobutamine. The coronary angiogram showed 90% stenosis of the right coronary artery. PTCA was performed on the lesion. Dobutamine stress echocardiography is useful for the diagnosis of myocardial ischemia in patients with implanted pacemakers.

We have studied the effects of MS-551 on the inward rectifier potassium channel (IK1) in isolated guinea-pig ventricular myocytes by use of whole-cell and single-channel recording techniques. MS-551 (5 microM) blocked the IK1 current. The percent blockade of the peak and steady-state IK1 current by MS-551 was constant at each test potential. In contrast 50 microM MS-551 failed to block either the sodium or the calcium current. Under cell-attached patch conditions, MS-551 reduced the open probability of IK1 channel activity by prolonging the interburst interval without changing either the unitary amplitude or the equilibrium potential. The blockade of IK1 was concentration-dependent. MS-551 did not change either the mean open time or mean closed time within a burst. Extracellular acidification (pH 6.4) strongly attenuated the effect of MS-551 on the open probability of IK1 channel activity when compared with its effect at pH 7.4. In summary, our results demonstrated that MS-551 blocked the IK1 channel. The neutral form of this drug molecules may penetrate the cardiac cell membrane via a hydrophobic pathway to block the steady-state IK1 current by reduction of open probability.

Left isomerism with critical arrhythmia in a 34-year-old housewife is reported. Left isomerism is rare among adult congenital disorders. The prognosis in childhood depends on intractable heart failure, but is unclear in adulthood. We describe an adult patient with left isomerism who recovered from life-threatening arrhythmias. Transesophageal echocardiography was especially useful to identify the morphology of both atrial appendages.

The diagnostic usefulness of dipyridamole-stress two-dimensional echocardiography was assessed in 82 patients consisting of 27 patients with angina pectoris, 42 with myocardial infarction, and 13 control subjects. Two-dimensional echocardiographic monitoring was performed during dipyridamole infusion: 0.56 mg/kg for 4 minutes, then discontinuation for 4 minutes, followed by a final infusion of 0.28 mg/kg for 2 minutes. The cumulative dose was 0.84 mg/kg. Worsening or fixed wall motion abnormality with unaffected baseline indicated a positive finding. All patients underwent coronary angiography. The sensitivity and specificity of dipyridamole-stress two-dimensional echocardiography for diagnosis of significant coronary artery stenosis (or = 75%) were 84% (58/69) and 92% (12/13), respectively. The sensitivity of this method for the branches of the coronary artery was 85% for the left anterior descending artery, 80% for the right coronary artery, and 75% for the left circumflex artery. The sensitivity for single-, double-, triple-vessel disease was 75%, 81% and 100%, respectively. The sensitivity and specificity of the dipyridamole electrocardiogram (ST depression more than 0.1 mV) were 33% (23/69) and 77% (10/13), respectively. The appearance of dipyridamole-stress induced wall motion abnormality was significantly earlier than those of chest pain and ST segment depression. Side effects were observed in 43% (35/82) of patients, but were only mild and transient. Dipyridamole-stress two-dimensional echocardiography is the best method for detecting coronary artery stenosis and predicting the localization of lesion sites.

To determine the necessity of sodium channel fast inactivation for the block of sodium current (INa) by disopyramide, we studied the effects of disopyramide on INa in guinea pig ventricular myocytes treated with chloramine-T, which removes the fast component of INa inactivation. After exposure to chloramine-T (2 mM), INa amplitude was reduced at all voltages and INa decay was irreversibly prevented. Disopyramide (20 microM) produced both tonic block and use-dependent block of INa in chloramine-T-treated myocytes. Before treatment with chloramine-T, the time course of both the onset of and recovery from use-dependent block by disopyramide were best fit by the sum of double exponential functions, and the time constant of the slow phase of recovery increased as the membrane was hyperpolarized. After removal of the fast component of INa inactivation by chloramine-T, the fast phase of the onset block and the fast phase of recovery from block were abolished. However, the voltage dependency of the time course of recovery from block was unchanged. Thus, although the fast sodium inactivation process is not required for tonic and use-dependent block of INa by disopyramide, it contributes to the fast phase of block development and unbinding from use-dependent block.

Eighteen patients with essential hypertension received 50 to 200 mg of dilevalol or 60 to 90 mg of propranolol daily for six weeks. Mean arterial blood pressure and venous pressure were significantly reduced in the dilevalol-treated patients at six weeks but were unchanged in the propranolol-treated patients. The cardiac index and systemic vascular resistance remained unchanged in the dilevalol group, but were significantly reduced (cardiac index) or increased (systemic vascular resistance) in the propranolol group. No changes in heart rate were noted in either treatment group. It is concluded that dilevalol has some ideal features for the treatment of hypertension, but further research is needed to determine the causes of fatal hepatotoxicity reported in a few cases.

The purpose of this study was to evaluate the antihypertensive effect of a new calcium antagonist, clentiazem, on inpatients or outpatients with essential hypertension. After blood pressure was stable and greater than 160/95 mmHg with placebo for at least a 2-week observation period, oral clentiazem was administered once daily and dosage was increased stepwise from 10 to 40 mg over 10 weeks. Blood pressure significantly decreased by the second week of the study, and this hypotensive effect was maintained until the eighth week. Cumulative effective rate (percent of patients whose blood pressure decreased in 20/10 mmHg) in 62 outpatients were as follows; 10.3% at 10 mg, 39.6% at 20 mg, 70.2% at 30 mg, 76.6% at 40 mg. There was no significant postural change observed in the blood pressure from supine to standing position. Side effects such as dizziness, general malaise and gait disturbances were observed in 3 (3.9%) of 76 patients. No abnormal changes in clinical laboratory examinations or electrocardiograms were caused by clentiazem. Thus these data demonstrated that clentiazem produces certain antihypertensive effects with sufficient safety.

The effects of nitroglycerin (NTG) on relaxation characteristics of the infarcted and non-infarcted myocardium were investigated by calculating a segment length on the epicardium of the left ventricle for 16 patients with old myocardial infarction. The spatial segment length was measured between two points which were identified as a junction of ramifying branches of the left coronary arteries using biplane coronary cineangiography. Regional myocardial stiffness was expressed as delta P/delta L, where delta P was an increment of left ventricular (LV) diastolic pressure from the lowest LV diastolic pressure to the pressure at the maximal segment length, and delta L was the difference of two segment lengths corresponding to those pressures. Myocardial stiffness decreased from 0.0402 +/- 0.0293 mmHg/mm to 0.0212 +/- 0.0157 with intracoronary NTG (p less than 0.01) and from 0.0220 +/- 0.0090 to 0.0136 +/- 0.0124 with sublingual NTG (p less than 0.001) in the non-infarcted portions. However, it was unchanged with both intracoronary and sublingual NTG in the infarcted portions. NTG may cause venous pooling and may decrease diastolic wall tension of the left ventricle as its indirect effect on the non-infarcted myocardium. Also, the non-infarcted myocardium may be influenced by dilatation of the epicardial coronary artery. Muscle stiffness of the infarcted myocardium was unchanged, probably due to the rigidity of myocardial fibrosis. It was concluded that in myocardial infarction diastolic distensibility of the non-infarcted portion can be improved by NTG both through indirect and direct effects.

In 16 patients with angina pectoris who had no histories of myocardial infarction, myocardial segment shortening was studied during angina-free periods. Myocardial segment length in the anterior wall of the left ventricle was calculated by measuring the spatial length between two points identified as junctions of ramifying branches of the left coronary arteries using biplane coronary cineangiography. Segment shortening was classified according to the severity of coronary arterial stenosis. The patients were categorized according to the severity of coronary arterial stenosis: as 1) the 0% stenosis (normal); 2) the 50% stenosis group; and 3) the 75-90% stenosis group. Total segment shortening in the normal group was the same as that in the 50% stenosis group (10.4 +/- 2.5%). However, in the 75-90% stenosis group, segment shortening was reduced to 7.3 +/- 2.5%. Effective segment shortening during the ejection period was reduced (5.0 +/- 1.8%) in the 75-90% stenosis group, as compared with the normal group (8.4 +/- 2.4%) and the 50% stenosis group (7.2 +/- 3.6%). This study demonstrated that segment shortening was reduced at rest in patients with angina pectoris who had had no previous infarction. A possible mechanism of this reduced segment shortening during angina-free periods may be irreversible myocardial alteration from recurrent ischemic attacks.

Left ventricular wall motion in patients with hypertrophic cardiomyopathy may show a characteristic movement since this condition is characterized by a disproportionate thickening of the wall and disorientation of myocardial muscle fibers. Biplane coronary cineangiograms were performed in 5 patients with hypertrophic cardiomyopathy and the spatial distance between the bifurcation of the left coronary artery was calculated using a digitizer-computer-plotter system as a measure of epicardial chord segment length. Systolic shortening of the segment was calculated as (LECG R--LES)/ECG R x 100 (%), where LECG R and LES represent segment lengths at the R wave of the electrocardiogram and at the end of systole, respectively. The value amounted 6.9 +/- 5.1 (+/- SD)% on the average which was significantly lower than the previously described values (9.0 +/- 4.1%) in 19 normal subjects. In all of 3 segments at the apex, systolic shortening showed nearly zero or negative indicating systolic expansion. Reduced shortening in patients with hypertrophic cardiomyopathy observed at the epicardial segment in the present study might be a reflection of geometrical difference between endocardial and epicardial segments because shortening of the epicardium will be reduced even the endocardium shortens considerably if the thickness of the wall is markedly increased. Anterior surface of the interventricular septum might be unable to shorten freely along the long axis since it is a junction of trifurcation among right and left ventricular free walls and the interventricular septum if these three walls are thickened. The present study indicated that shortening characteristics in the outer myocardium in patients with hypertrophic cardiomyopathy is markedly impaired possibly due to geometrical difference between endocardial and epicardial segments caused by marked thickening of the wall and also due to the degeneration or disorientation of myocardial fibers.

A mechanism for the genesis of early relaxation of the left ventricle was assessed. For 18 patients with coronary artery disease, biplane left coronary cineangiography was performed and the coordinates (x, y, z) of the points of the artery were measured by frame to frame basis throughout one cardiac cycle. The spatial distance (segment length) between any two points was calculated on each frame as (Formula: See text) to investigate shortening and relaxation characteristics of the ischemic and nonischemic segments. Coronary angiography was repeated during right atrial pacing to aggravate ischemia, and following nitroglycerin administration to ameliorate ischemia. From data of six normal subjects, 43 segments were calculated. All showed shortening during systole and lengthening in diastole. Right atrial pacing caused early relaxation in only two of the 43. Two hundred and fifteen segments were calculated for 18 patients with coronary artery disease. All but eight segments showed normal relaxation on control angiography. Following pacing, 115 segments showed early relaxation, and in 107 of the 115, normal relaxation were restored after nitroglycerin. Among the 107 segments, 44 were ischemic and 63 were normal. For 34 segments with early relaxation by pacing, pacing was repeated after administering nitroglycerin, and 15 did not reproduce early relaxation. The present study showed that early relaxation was observed in patients with coronary artery disease, which was effectively ameliorated by nitroglycerin, suggesting this phenomenon is closely related to the development of myocardial ischemia. The decreased active tension, reduced duration of tension, development and delay in electrical depolarization in the ischemic segment can be a reasonable inducement to early relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

The shift of the heart during systole within the thorax was measured using bifurcations of the left coronary artery as cineangiographic markers. Biplane coronary cineangiography was performed in 13 normal subjects and 6 patients with non-obstructive hypertrophic cardiomyopathy (HCM). The spatial coordinates (X, Y, Z) of the bifurcations on the cineangiograms were measured using a motion analizer-digitizer-computer system. The systolic excursion of the motion of a bifurcation located at the anterior-basal point of the heart was 1.4 +/- 0.1 (+/-SD) cm leftward, 3.0 +/- 0.3 cm caudally and 2.5 +/- 0.1 cm anteriorly in normal subjects. In the cases with HCM, on the other hand, the bifurcation moved 2.2 +/- 1.1, 2.7 +/- 1.2 and 2.2 +/- 0.6 cm during systole, respectively. The movement at the apex in the normal subjects was 1.7 +/- 0.2 cm rightward, 1.5 +/- 0.2 cm caudally and 1.5 +/- 0.2 cm posteriorly, although the direction was reversed as compared to that of the anterior wall of the cardiac base. The amplitude of the excursion was also reduced at the apex, suggesting the systolic twist of the ventricular wall. The excursion of the apex in HCM was 0.6 +/- 1.7, 1.5 +/- 1.8 and 2.5 +/- 1.4 cm, respectively, toward the base of the heart as in the normal subjects. The maximum speeds of these motions were 34.0 +/- 9.2 cm/sec leftward, caudally and anteriory at the anterior-basal point and 36.2 +/- 7.3 cm/sec rightward, caudally and posteriorly in the normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

In 8 dogs, several paired lead beads as radiopaque markers were implanted in the subepicardial and subendocardial regions, and biplane cineradiograms were obtained after closure of the chest. The spatial distance (segment length) between the two markers in the outer and inner sides of the myocardium was calculated using a digitizer-computer-plotter system, and the effect of nitroglycerin on regional left ventricular geometry was assessed. Segment length at the R wave of the electrocardiogram (LECG R) was reduced from 39.7 +/- 11.8 (mean +/- SD) to 38.8 +/- 12.1 mm at the subepicardium and from 31.9 +/- 9.5 to 29.5 +/- 10.4 mm at the subendocardium 3 minutes after intravenous injection of 0.5 mg of nitroglycerin. Segment length at endsystole (LES) was also reduced from 38.9 +/- 11.7 to 38.2 +/- 11.8 mm at the subepicardium and from 29.6 +/- 9.2 to 27.9 +/- 9.9 mm at the subendocardium by nitroglycerin. Systolic shortening [(LECG R--LES)/LECG R] x 100) showed a slight reduction after nitroglycerin. Left ventricular wall thickness measured as a distance between subepicardial and correspondent subendocardial markers showed a slight but significant increase by nitroglycerin: Maximal thickness was increased from 10.9 +/- 3.2 to 11.4 +/- 3.3 mm, and thickness at the R wave of the electrocardiogram was also increased from 10.9 +/- 3.1 to 10.5 +/- 3.2 mm. Thickening of the wall was markedly increased at the anterior mid portion of the left ventricle but not at the base, suggesting nitroglycerin has larger effect on the former position than the latter.

This study was performed to clarify the difference of shortening characteristics between left ventricular epicardium and endocardium. Four to five pairs of radiopaque markers (lead beads, phi 0.3- 0.8 mm) were implanted just beneath the epicardium and endocardium, respectively in eight open-chest dogs. After the pericardium and thorax were closed, biplane cine-roentgenograms were obtained. The spatial distance (segment length) between any two of the markers was calculated using a digitizer-computer-plotter system. Left ventricular wall thickness (Th) was measured as a distance between epicardial and endocardial markers. The maximum left ventricular thickness (Thmax) was 9.4 +/- 3.4 mm (mean +/- SD), the minimum (THmin) 8.4 +/- 3.1 mm, and a percent increase of wall thickness [(Thmax-Thmin)/Thmin] was 12.7 +/- 6.5%. The value of epicardial segment length divided by endocardial segment length as normalized by each length at R wave of ECG was 1.088 +/- 0.071 at the end of systole and 0.979 +/- 0.016 at end diastole, indicating that endocardial segment shortened and distended more than epicardial segment during systole and diastole, respectively. Epicardial segment began to shorten 3 +/- 26 msec earlier and distend 4 +/- 50 msec earlier than endocardial one. This study revealed a small but consistent difference in the amount of shortening and its initiation and termination between the epicardium and endocardium.

The left ventricular diastolic properties of patients with hypertrophic cardiomyopathy are impaired. Since there is degeneration or disarray of myocardial fibers in patients with hypertrophic cardiomyopathy (HCM), the rate of expansion in diastole may become asynchronous. Biplane coronary cineangiograms were performed in eight normal subjects and nine patients with HCM. The coordinates (x,y,z) of the ramifying points of the left coronary artery were measured, and the distance between any two of the points of the coronary artery was calculated (segment length). Fifteen segment lengths were calculated for each subject. Since the onsets of expansion of these 15 segment lengths were not simultaneous, they expanded at different times and the onsets of expansion occurred within a very short period of time, nearly at end-diastole. The variance (standard deviation) of the timing of expansions of these 15 segments and the rate of expansion within the late 40 msec of the isovolumic relaxation period (% delta L) were calculated. The time constant of the left ventricular pressure fall (T) in normal subjects was 41.3 +/- 7.7 (SD) msec, T in HCM was prolonged to 52.7 +/- 11.1 msec. The variance was 47 +/- 17 msec in normal subjects, but it increased to 99 +/- 26 msec in HCM. The rate of expansion again decreased in HCM (Normal 2.24 +/- 0.60 vs HCM 1.40 +/- 0.96%). The conspicuous diastolic asynchrony in the onset of expansion and the reduced rate of diastolic expansion in HCM may be the mechanism of impairing the diastolic properties of the left ventricle.

In order to investigate relaxation characteristics of the infarcted wall, segment lengths of the left ventricular wall were calculated in 6 patients with anterior myocardial infarction and in 9 angiographically normal subjects. The biplane left coronary cineangiography was performed and coordinates of ramifying points of the left coronary artery on the infarcted or non-infarcted wall were measured and the spatial lengths (segment lengths) on each wall were calculated. If the two points are on the left anterior descending artery (LAD) in infarcted patients, a calculated length is regarded as a segment length in the infarcted portion, while if the length is calculated between the two points located on the coronary artery other than LAD, it is a non-infarcted segment. Each segment length was calculated in frame by frame covering one cardiac cycle. The maximum length (Lmax), minimum length (Lmin) and the length at the beginning of P wave of the electrocardiogram (LECG P) were calculated. The extent of relaxation of the segment caused by atrial kick was calculated as (Lmax--LECG P)/Lmax X 100, (% delta Lla). This value was 2.8 +/- 1.5 and 3.5 +/- 1.4% on anterior and inferior walls, respectively, in 9 normal subjects and 3.6 +/- 1.2 and 4.0 +/- 0.9% in 6 patients with anterior infarction, revealing no significant difference among 4 values. This indicates that the amount of lengthening of the segment by atrial kick remains unchanged even if the wall is infarcted. The extent of diastolic lengthening of the segment by rapid and slow fillings, which excludes atrial filling, was calculated as (LECG P--Lmin)/Lmax X 100, (% delta L1-la).(ABSTRACT TRUNCATED AT 250 WORDS)

Several methods of digital subtraction angiography (DSA) were compared to determine which could better visualize regional myocardial perfusion using coronary angiography in seven patients with myocardial infarction, two with angina pectoris and five with normal coronary arteries. Satisfactory DSA was judged to be achieved if the shape of the heart on the mask film was identical to that on the live film and if both films were exactly superimposed. To obtain an identical mask film in the shape of each live film, both films were selected from the following three phases of the cardiac cycle; at the R wave of the electrocardiogram, 100 msec before the R wave, and 200 msec before the R wave. The last two were superior for obtaining mask and live films which were similar in shape, because the cardiac motion in these phases was relatively small. Using these mask and live films, DSA was performed either with the continuous image mode (CI mode) or the time interval difference mode (TID mode). The overall perfusion of contrast medium through the artery to the vein was adequately visualized using the CI mode. Passage of contrast medium through the artery, capillary and vein was visualized at each phase using TID mode. Subtracted images were displayed and photographed, and the density of the contrast medium was adequate to display contour lines as in a relief map. Using this DSA, it was found that regional perfusion of the contrast medium was not always uniform in normal subjects, depending on the typography of the coronary artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular size at different portions was evaluated following the administration of nitroglycerin to find whether there is any regional difference in the amount of shortening. In 6 patients with old myocardial infarction, biplane coronary cineangiograms were obtained before and after sublingual administration of nitroglycerin of 0.3 mg. The coordinates of the bifurcations of the left coronary artery at multiple sites were measured on the postero-anterior and lateral films and the spatial lengths (L) between any paired two points were calculated frame by frame covering one cardiac cycle. The maximum length (Lmax) was 63.2 +/- 3.1 (SE) mm before nitroglycerin as a whole and was 61.4 +/- 2.9 mm after nitroglycerin, showing no significant change. The minimum length (Lmin) also showed no significant change after nitroglycerin; from 56.1 +/- 2.9 to 54.9 +/- 2.6 mm. However, at the free wall, Lmax after nitroglycerin was reduced by 4.5 +/- 2.5%, and Lmax at the anterior septum was also reduced by 3.0 +/- 1.3%. Lmax at the base was unchanged after nitroglycerin. Lmin at the free wall and at the anterior septum were also reduced after nitroglycerin, 4.4 +/- 2.6 and 2.9 +/- 1.2%, respectively, and it was unchanged at the base. Since a reduction in the left ventricular size is effective in reducing myocardial oxygen demand and is effective in treating myocardial ischemia, it was suggested that nitroglycerin is more effective in relieving ischemia at the free wall and septum and less effective at the base.