Coronary artery spasm induced in atherosclerotic miniature swine.

Angiographically demonstrable coronary artery spasm could be provoked repeatedly by giving intracoronary or intravenous injections of histamine to miniature swine with experimentally induced atherosclerotic lesions of the coronary artery. The spasm induced in this way subsided either spontaneously or after the administration of nitroglycerin and was prevented by a calcium antagonist or an agent that blocks histamine H1 receptors. This model, which suggests that atherosclerotic changes may be one of the primary factors in the occurrence of coronary artery spasm, should facilitate studies on the pathogenesis of this condition.

Histamine-induced spasm not significantly modulated by prostanoids in a swine model of coronary artery spasm.

The role of prostanoids in a swine model of coronary artery spasm was examined. Eighteen miniature pigs underwent endothelial denudation of the left coronary artery (left circumflex branch in 14 pigs and left anterior descending branch in 4 pigs) followed by high cholesterol feeding. Three months after the denudation, when coronary artery spasm was repeatedly provoked along the denuded portion of the coronary artery by histamine, the vasoconstrictive effect of thromboxane A2 and the preventive effects of indomethacin and prostacyclin against histamine-induced coronary artery spasm were examined. Intracoronary administration of thiothromboxane A2, 200 micrograms, a stable thromboxane A2 analog, failed to provoke coronary artery spasm (seven of seven cases) but nonselectively constricted the coronary artery by 33%. Intravenous administration of indomethacin, 2 mg/kg, or continuous intravenous infusion of prostacyclin, 50 ng/kg per min, failed to prevent histamine-induced coronary artery spasm (four of four and eight of eight cases, respectively), yet the spasm was all but prevented by intravenous pretreatment with diphenhydramine at a dose of 1 mg/kg. Thus, in this swine model, prostanoids may not play a primary role in the occurrence of coronary artery spasm.

New echocardiographic observations in a patient with dissimilar atrial rhythms.

A patient with an impure flutter was found to have dissimilar atrial rhythms that were confirmed by direct ECG recordings. Echocardiographic studies disclosed that the a waves on the mitral echocardiogram occurred synchronously with the a waves on the esophageal ECG that, in turn, showed atrial flutter at a rate of 300 beats per minute. However, the a waves on the tricuspid echocardiogram coincided closely with the P waves on a surface ECG (lead V) that disclosed a chaotic atrial tachyarrhythmia. These results suggest that echocardiographic study, in conjunction with an esophageal ECG, may be a useful, noninvasive technique for the diagnosis of dissimilar atrial rhythms.

Collateral function modified by glyceryl trinitrate and dipyridamole during coronary occlusion in conscious dogs.

The effects of glyceryl trinitrate and dipyridamole on induced ischaemia were studied in awake dogs during transient coronary occlusion before and after collateral development. Seventeen dogs were instrumented under sterile conditions with a miniature pressure gauge to measure left ventricular pressure, a cannula for aortic pressure, and pairs of piezoelectric crystals towards the subendocardium of the left ventricle for regional segment length measurements. A hydraulic cuff occluder and Doppler flow probe were placed around the left circumflex coronary artery. Collateral function was increased by repeated 2 min coronary occlusions at 32 min intervals for 2-9 days until regional wall motion returned to preocclusive values, despite the persistence of coronary occlusion. The effects of glyceryl trinitrate and dipyridamole were studied after the initial haemodynamic changes had subsided. Collateral function was quantified by integrating changes in end systolic length of the ischaemic area during coronary occlusion. Before collateral development the end systolic length area was 29.4(2.4) cm X s and was unchanged by glyceryl trinitrate or dipyridamole. After the development of collaterals the end systolic length area decreased from 4.1(1.1) to 2.2(1.0) cm X s (p less than 0.01) after glyceryl trinitrate and increased to 14.9(1.7) cm X s (p less than 0.01) after dipyridamole. Therefore, glyceryl trinitrate acted directly on collaterals and improved the induced ischaemia, whereas dipyridamole exaggerated the regional wall motion abnormality.

Tricuspid valve endocarditis in a non-drug addict associated with peliosis hepatis.

A 31-year-old woman was admitted because of persistent remittent fever. Tricuspid valve endocarditis due to Staphylococcus aureus was identified as the cause of fever. The patient had no history of intravenous drug abuse, oral contraceptives or predisposing cardiac disease. Huge hepatomegaly was found without any signs of congestive heart failure. Liver enzyme abnormalities were not detected throughout the entire course of therapy. The liver biopsy specimen revealed peliosis hepatis. Treatment with panipenem/betamipron was successful, although recurrent septic pulmonary embolism occurred. The cause of the huge hepatomegaly encountered in the present case may be attributable to peliosis due to severe infection.

[Quantification of myocardial infarct size by technetium-99m pyrophosphate single photon emission computed tomography].

Myocardial infarct size in 41 patients with the first attack of acute transmural myocardial infarction (MI) was assessed by technetium-99m pyrophosphate single photon emission computed tomography (99mTcPYP-SPECT). A ratio of the number of voxels of 99mTcPYP uptake into the infarct area to that into the thorax was calculated as a parameter of MI size. The ratio was positively correlated with both peak CPK activity (r = 0.53, p less than 0.005, n = 24) and extent score in 201TI-SPECT (r = 0.70, p less than 0.005, n = 14) significantly in patients with anterior MI but not in patients with inferior MI. There was also significant negative correlation between the ratio and the left ventricular ejection fraction (LVEF) measured by RI angiography in both acute (r = -0.67, p less than 0.005, n = 18) and chronic (r = -0.75, p less than 0.005, n = 25) phases in patients with anterior MI. Recovery in LVEF at chronic phase was noted in patients with small anterior MI but not with large anterior MI. 8 of 14 patients with inferior MI had right ventricular MI, that might have affected evaluation of MI size and resulted in no correlation between variables. It was suggested that 99mTcPYP-SPECT was a useful method to evaluate MI size and to predict prognosis of cardiac function in patients with anterior MI but not in patients with inferior MI.

[A case of lupus erythematosus preceded by right heart failure due to pulmonary hypertension].

A 40-year-old woman was admitted because of increasing exertional dyspnea. Right heart failure was suggested by the presence of hepatomegaly, pretibial edema and also echocardiographic findings. Physical examination and echocardiography showed no evidence of valvular disease or congenital heart disease except for right ventricular dilatation and tricuspid regurgitation. The ventricular septum deviated toward the left ventricle throughout the cardiac cycle, but left ventricular function was preserved. Severe pulmonary hypertension averaging 44 mmHg was revealed by cardiac catheterization. Digital subtraction angiography and pulmonary blood flow scintigraphy showed no evidence of pulmonary artery embolism, and no interstitial pulmonary lesions that might have caused pulmonary hypertension were recognized. Hypergammaglobulinemia suggested an autoimmune disorder, and signs of systemic lupus erythematosus (SLE), such as pleural effusion, proteinuria, lymphocytopenia, LE cell phenomenon and antinuclear antibodies were present. Several autoimmune diseases are known to be causative factors of pulmonary hypertension. However, only ten cases of SLE complicated by pulmonary hypertension have been reported the present one. These cases were characterized by a high incidence of Raynaud's phenomenon and positivity for anti-RNP antibody. In our present case, SLE activity was suppressed using prednisolone, but pulmonary hypertension persisted and the patient eventually died due to right cardiac failure. Judging from the clinical course of the ten reported cases of SLE-pulmonary hypertension, there seems to be no hope of improving the pulmonary hypertension once it has become established. Therefore it is important to detect and cure pulmonary hypertension as early as possible.

Coronary artery spasm induced in miniature swine: angiographic evidence and relation to coronary atherosclerosis.

In a swine model of coronary artery spasm, the pathogenetic role of coronary atherosclerosis was examined. Following endothelial balloon denudation of the left circumflex coronary artery (LCX), male miniature swine were fed a laboratory chow diet containing 2% cholesterol. Although there was no difference in the extent of coronary vasoconstrictive response to histamine, serotonin, and ergonovine between the left anterior descending coronary artery (LAD) and the LCX before the denudation, a constrictive response was significantly augmented along the denuded portion of the LCX 1 and 3 months after the denudation. Augmented vasoconstrictive responses to phenylephrine were never evidenced. Histamine was the most potent vasoactive agent, and coronary artery spasm was provoked repeatedly by intracoronary or intravenous administration of histamine in the presence or absence of cimetidine. The spasm was provoked only in the denuded portion of the LCX, the same area which was angiographically normal before the occurrence of the spasm. Histologically, atherosclerotic changes were predominant along the denuded portion of the LCX. Topologic correlation was suggested between the site of the spasm and the site of coronary atherosclerosis. It is concluded that in this swine model of coronary artery spasm, atherosclerotic changes may be an important causative factor, in terms of an activation of multiple receptor-operated calcium channels in the coronary artery.

Wall motion abnormalities in Q wave and non-Q wave myocardial infarction in isolated left anterior descending coronary artery disease.

Although the frequencies of transmural involvements of Q wave and non-Q wave myocardial infarction (MI) are similar, their clinical features are different in many aspects. In the present study, the wall motion abnormalities of 34 patients with Q wave MI and eight patients with non-Q wave MI, all with isolated left anterior descending artery (LAD) lesion, were compared using left ventriculography and two-dimensional echocardiography. This study clearly demonstrated that the severity and distribution of asynergy were significantly greater in patients with Q wave MI than in those with non-Q wave MI. Akinesis or dyskinesis was observed in all 34 patients (100%) (151 of 544 segments) with Q wave MI, and in four of eight patients (50%) (eight of 128 segments) with non-Q wave MI (p less than 0.05). Apical aneurysm occurred exclusively in patients with Q wave MI. In non-Q wave MI, asynergy was localized at the papillary muscle level or the apex. At the chordal level, asynergy was observed in only one of eight cases with non-Q wave MI, and in 24 of 34 cases with Q wave MI (p less than 0.05). These results suggest that the infarct size may be smaller in non-Q wave MI than in Q wave MI in patients with isolated LAD lesion.

Pseudo-knock sound in a patient with nephrotic syndrome and massive ascites.

A patient with markedly elevated diaphragm due to massive ascites secondary to nephrotic syndrome demonstrated an intense early diastolic sound with low- and medium-pitch. This abnormal sound coincided closely with the "D" point of the anterior mitral valve echogram. This sound remarkably diminished in intensity during inspiration with lowering of diaphragm, and after removing ascites it completely disappeared. Noninvasive study with phonoechocardiograms showed neither constrictive pericarditis nor large pericardial effusion. These findings lead us to believe that the sound may be related to an abnormal ventricular recoil striking the extracardiac structures at the end of the isovolumetric relaxation time. To our knowledge, the fact that the elevated diaphragm itself can produce an early diastolic sound ("pseudo-knock sound") has not been previously reported.

Development of collateral function with repetitive coronary occlusion in a canine model reduces myocardial reactive hyperemia in the absence of significant coronary stenosis.

The present study was designed to elucidate the role of collateral development, per se, on reactive hyperemia without persistent coronary stenosis in instrumented conscious dogs. Functional states of coronary collaterals were augmented by repetitive 2 minutes of coronary occlusion every 30 minutes for 2-9 days. Regional shortening measured sonomicrometrically recovered from -1.2 +/- 6.5% of the preocclusive state at the end of the first coronary occlusion to 100.5 +/- 1.2% (n = 8, P less than 0.01) after repeated coronary occlusions. Before and after collateral development, transient coronary occlusions of 5, 10, 20, 30, 60, 90, and 120 seconds were randomly performed. The degree of regional dysfunction and the following reactive hyperemic response were measured. Up to 20 seconds of coronary occlusion, the flow ratio and duration of coronary reactive hyperemia increased similarly, both before and after collateral development. However, when the duration of coronary occlusion was over 30 seconds, flow ratio and debt repayment ratio were reduced progressively after the collateral development. Among the indices exhibiting reactive hyperemia, debt repayment ratio decreased initially and correlated well with the recovery of regional dysfunction during coronary occlusion. Thus, the augmentation of collateral function after repetitive coronary occlusion reduces reactive hyperemia even in the absence of significant coronary stenosis.

Effects of trapidil and nitroglycerin on coronary circulation in conscious dogs.

Effects of trapidil and nitroglycerin (glyceryl trinitrate) on coronary blood flow or epicardial coronary diameter were studied in conscious dogs, instrumented with a Doppler flow probe or a pair of ultrasonic dimension crystals on the left circumflex coronary artery. Bolus intravenous injections of trapidil (0.5, 1.0 and 2.0 mg/kg i.v.) increased coronary blood flow, dose-dependently, such being comparable at the peak value seen with nitroglycerin (5, 10 and 20 micrograms/kg i.v.). Coronary blood flow following the intravenous administration of trapidil or nitroglycerin increased biphasically and returned to pre-drug levels in 1.4 +/- 0.2 min (trapidil 1 mg/kg i.v.) or 1.0 +/- 0.1 min (nitroglycerin 10 micrograms/kg i.v.), while the mean coronary diameter increased monophasically and approached the control level 5 min after drug administration. The first peak was observed before the maximal decrease in aortic pressure and the second peak was associated with concomitant increases in heart rate and myocardial contractility induced by a sudden hypotension. Propranolol, a beta-blocker, did not modify the initial peak but attenuated markedly the second peak (P less than 0.05) in case of trapidil (1.0 mg/kg i.v.) or nitroglycerin (10 micrograms/kg i.v.), which corresponded with reduced changes in reflex tachycardia and positive inotropism. Therefore, the direct effects of trapidil and nitroglycerin on coronary circulation of conscious dogs are an initial transient dilatation of the resistance vessels followed by a continuation of the dilatation of the conductance coronary vessels.