Kohshiro Moritani

Effects of the presence or absence of preceding angina pectoris on left ventricular function after acute myocardial infarction

Left ventricular (LV) function was evaluated in 31 patients, who had total occlusion of the left anterior descending coronary artery and less than 70% stenosis of the other two major coronary arteries or any branch. Fifteen of 31 patients had a history of angina pectoris before acute myocardial infarction (AMI) and 16 of 31 patients had no history of angina pectoris before AMI. The patients with angina pectoris before AMI had a significantly better ejection fraction, percentage of abnormally contracting segment, and regional wall motion than those without angina pectoris before AMI. These data suggest that the symptom of angina pectoris before AMI could be a favorable sign in preserving LV function when the patients subsequently had AMI.

Determination of atrial size by esophageal echocardiography.

The sizes of both left atrial (LA) and right atrial (RA) cavities were assessed in 16 patients by esophageal echocardiography and biplane cineangiography. The changes in echocardiographic dimension and cineangiographic volume during 1 cardiac cycle showed excellent correlations in both atria. In the left atrium, the relation between the echocardiographic dimension and the cineangiographic volume was significant (r = 0.83) and was fitted by the following power function: LA volume (ml) = 0.94 X LA dimension (mm) 1.24. In the right atrium, the relation between the dimension and the volume was significant; RA volume (ml) = 0.015 X RA dimension (mm) 2.34 (r = 0.95). Thus, esophageal echocardiography is a useful method for evaluating LA and RA size and simultaneously observing of both atria.

Coronary angiography during exercise-induced angina with ECG changes

Coronary angiography was performed at rest and during bicycle exercise immediately after the onset of angina and significant ST segment elevation or depression in the ECG. Of 11 patients, six showed significant reduction of coronary lumen diameter at the site of organic stenosis; mean values of stenosis (range) before and during exercise were 55% (25% to 88%) and 98% (89% to 100%), respectively. Five patients did not have any diameter change of the organic lesion; mean values of stenosis (range) before and during exercise were 84% (74% to 89%) and 84% (73% to 92%), respectively. Excluding the areas of these stenoses, diameters of left main coronary artery, proximal, middle, and distal left anterior descending, circumflex, and right coronary artery segments were measured before and during exercise. Diameter in each coronary artery segment during exercise was not significantly changed from that before exercise, both in the groups with and without diameter reduction. Exercise provoked a localized worsening of coronary artery stenosis without changing the diameter in the remaining artery. These findings suggest that the worsening of stenosis might be caused by a regional abnormality of the coronary artery that is not necessarily related to the degree of organic stenosis.

Angina pectoris before and during acute myocardial infarction: Relation to degree of physical activity

One hundred ninety-seven patients with a history of acute myocardial infarction (AMI) were interviewed to evaluate the character of angina pectoris relative to physical activity before AMI and at the onset of AMI. Ninety-two patients had no angina before AMI and 105 had angina. Among the 105 patients with angina, 58 had chronic stable angina that did not change before AMI, 22 noted worsening of symptoms within 2 weeks before AMI, and 25 had onset of angina within 2 weeks before AMI. In the 92 patients without angina before AMI, AMI occurred during heavy exertion in 10 (11%), mild exertion in 43 (47%), at rest in 28 (30%), and during sleep in 11 (12%). In the 58 patients with chronic stable angina, 47 had angina during exertion, 7 during rest and 4 during both. However, subsequent AMI occurred during heavy exertion in 9 (15%), during mild exertion in 16 (28%), at rest in 25 (43%), and during sleep in 8 (14%). In the patients without angina, or with chronic stable angina without worsening of symptoms, AMI occurred unpredictably or differently from the mode of physical activity precipitating angina before AMI.

Efficacy of N-acetylcysteine and aminophylline in preventing contrast-induced nephropathy

BACKGROUND Contrast-induced nephropathy (CIN) is one of the important complications of coronary angiography (CAG) and percutaneous coronary intervention (PCI), especially in patients with chronic kidney disease (CKD). Prophylactic administration of N-acetylcysteine (NAC) and aminophylline has been reported to be effective in some trials, but the results still remain controversial. We investigated the efficacy of NAC or aminophylline in preventing CIN. METHODS AND RESULTS Forty-five consecutive patients undergoing CAG and/or PCI were randomly assigned to receive hydration and NAC (704 mg orally twice daily; NAC group, n=15), hydration and aminophylline (250 mg intraveneously 30 min before CAG and/or PCI; aminophylline group, n=15), or hydration alone (control group, n=15). We compared serum creatinine (SCr), creatinine clearance (Ccr), blood beta-2 microglobulin, and urinary beta-2 microglobulin levels at baseline and 48h after CAG and/or PCI. In the NAC group, SCr decreased from 1.00 + or - 0.36 to 0.67 + or - 0.16 mg/dl (p<0.01), and Ccr significantly increased from 62.4 + or - 15.6 to 80.4 + or - 8.39 ml/min (p<0.01). In the aminophylline group, SCr and Ccr were unchanged. In the control group, SCr significantly increased from 0.94 + or - 0.21 to 1.28 + or - 0.21 mg/dl (p<0.01), and Ccr significantly decreased from 63.7 + or - 16.1 to 46.1 + or - 10.6 ml/min (p<0.01) after CAG and/or PCI. In the NAC group, mean blood beta-2 microglobulin significantly decreased from 2.38 + or - 0.58 to 1.71 + or - 0.38 mg/dl (p<0.01), and in the aminophylline group, mean urinary beta-2 microglobulin concentration significantly decreased from 337 + or - 31.0 to 239 + or - 34 microg/ml (p<0.01). CONCLUSIONS These results suggest that both prophylactic NAC and aminophylline administration are effective in preventing CIN, but not with hydration alone. It appears that the two compounds work in different ways against CIN.

Response of the coronary artery to a small dose of ergonovine in variant angina

The response of the coronary artery to a small dose (0.01 mg) of ergonovine was observed in nine patients without variant angina and in 10 patients with variant angina. Coronary angiograms were obtained before and after small and larger (routinely used) doses of ergonovine. With the larger dose, all 10 patients with variant angina had total or subtotal spastic occlusion accompanied by angina and ECG changes. Excluding the site of spastic occlusion produced by the larger dose of ergonovine, diameters of proximal, middle, and distal segments in each major coronary artery were measured before and after a small dose of ergonovine. The mean percentage of change in diameter (diameter before - diameter after a small dose of ergonovine)/diameter before a small dose of ergonovine X 100% in patients without variant angina was not significantly different from that in patients with variant angina (5.2 +/- 9.5% vs 7.0 +/- 11.9%, respectively). However, in patients with variant angina, a small dose of ergonovine produced a percentage of change in diameter of 39.8 +/- 15.3% at the site of spastic occlusion included by a larger dose of ergonovine, compared with that of 7.0 +/- 11.9% in the remaining non-spastic coronary arteries (p less than 0.05). These results indicate that patients with variant angina have local segments which respond differently to ergonovine from the remaining segments of coronary arteries. Clinically, this observation might be helpful in determining the angiographic positivity to ergonovine.

Transient appearance of collaterals during vasospastic occlusion in patients without obstructive coronary atherosclerosis

Coronary angiography of both right and left coronary arteries, using the Sones technique, was performed during the attack of total spastic obstruction in 11 patients with clinically documented history of variant angina. None of the patients had more than 70% stenosis of organic atherosclerosis in any coronary artery and none had a history of myocardial infarction. Total spastic obstruction occurred spontaneously in 3 of 11 patients, and was provoked by ergonovine maleate in eight patients. Six patients had total spastic obstruction in the left anterior descending coronary artery, four patients had total obstruction in the right coronary artery, and one patient had total obstruction in the left anterior descending and right coronary arteries. In 7 of 11 patients, the coronary artery distal to the total spastic obstruction received collaterals from the nonspastic artery. The collaterals disappeared promptly when the spastic coronary artery was patent. These patients had ST segment elevation in the ECG during the attacks. In the remaining four patients, the spastic artery did not receive any collaterals from the nonspastic artery, associated with ST segment elevation during the attacks. These findings suggest that the brief, repetitive total occlusion of the coronary artery may stimulate the enlargement of collaterals. These collaterals may not always function to prevent the ischemia of the myocardium on the ECG.

Analysis of digital subtraction coronary angiography for estimation of flow reserve in critical coronary stenosis

To examine the accuracy of digital subtraction angiographic assessment of coronary flow reserve in critical coronary stenosis, time-density curves were obtained from digital angiograms for a myocardial region of interest. Time-to-peak contrast (TPC) and contrast washout rate (T) were measured in 11 patients with critical 1-vessel lesions before and after percutaneous transluminal coronary angioplasty (PTCA). Collectively, the values of TPC and T were significantly shortened, from 5.8 +/- 1.1 to 4.4 +/- 1.0 seconds (p less than 0.01) and from 11.3 +/- 4.0 to 5.2 +/- 1.2 seconds (p less than 0.001) after PTCA, respectively. All 11 patients except 1 showed shortened T after PTCA; however, in 5 of the 11 patients, TPC after PTCA had approximately the same values as those before PTCA. In experiments in dogs with critical circumflex stenosis, coronary flow and posterior wall thickening at rest were not different from control; however, contrast media-induced hyperemia was markedly attenuated, accompanied by a significant prolongation of T (7.7 +/- 4.5 vs 15.8 +/- 1.9 seconds, p less than 0.01) and completely unchanged TPC (both 6.8 seconds). With simultaneous tracings of coronary flow and time-density curves, TPC and the washout phase on the curve corresponded with contrast-induced transient flow reduction and hyperemic phases, respectively. It is concluded that T appears more sensitive than TPC when basal coronary flow is maintained to almost normal levels, as in patients with stable effort angina pectoris having critical coronary stenosis.

Left ventricular wall motion at rest in patients with organic coronary artery disease vs coronary spasm.

Left ventricular ejection fractions and regional ejection changes obtained from left ventriculograms at rest were analyzed in 15 normal subjects, in 17 patients with isolated, organic left anterior descending coronary artery disease, and in 11 patients with isolated left anterior descending coronary artery spasm. Patients with coronary artery spasm did not have significant organic lesions at the site of spasm. All patients with organic coronary artery disease and coronary artery spasm had a history of angina pectoris without myocardial infarction. No significant differences in ejection fraction were observed among the three groups. The regional ejection change of the anterolateral and apical wall supplied by the left anterior descending coronary artery was significantly decreased in patients with organic coronary artery disease compared with those in normal subjects (anterolateral 39.5 +/- 10.3% vs 48.4 +/- 7.7%, p less than 0.05; apical 48.4 +/- 8.8% vs 55.6 +/- 7.8%, p less than 0.05). However, the anterolateral and apical wall motion was not impaired in patients with coronary artery spasm. Thus, patients with organic coronary artery disease had impairment of left ventricular wall motion, while those with coronary artery spasm did not, although both groups of patients had symptoms of angina. These results suggest that patients with organic coronary artery disease may have had coronary blood flow disturbances through stenosed vessels and chronic active ischemia that produced left ventricular impairment.