Clinical, angiographic and anatomic findings in acute severe ischemic mitral regurgitation.

Severe mitral regurgitation (MR) due to coronary artery disease unfavorably alters prognosis for medical therapy and is also associated with increased surgical mortality. In this report, the clinical, angiographic and pathoanatomic findings in 50 consecutive patients with severe ischemic MR were characterized. Forty-two patients (84%) either presented with acute myocardial infarction or a well-documented prior infarction. Eleven patients (22%) were in cardiogenic shock at the time of catheterization. Forty patients (80%) had greater than 70% stenosis of the right and left circumflex coronary arteries with or without left anterior descending coronary artery stenosis. Segmental asynergy of the left ventricular wall was present in 48 patients (96%) and involved the inferior wall in 43 (86%). Mean ejection fraction for the group was 51 +/- 7%. A total of 15 patients had direct inspection of the mitral valve apparatus at surgery or autopsy. Posteromedial papillary muscle involvement was found in 14 patients, fibrosis or necrosis in 10 and rupture in 4, with anterolateral papillary muscle rupture in 1 patient. Thus, acute severe ischemic MR is usually associated with significant narrowing of both right and left circumflex coronary arteries, and posteromedial papillary muscle involvement.

Thrombosis-related markers in unstable angina pectoris.

While thrombus formation has been implicated in the pathogenesis of unstable angina, the value of thrombus-related markers for distinguishing unstable from stable angina is not well defined. Fibrin D-dimer and plasminogen activator inhibitor were prospectively analyzed in the peripheral blood of 46 patients (26 with unstable angina and 20 with stable angina or normal coronary arteries). Baseline blood samples were drawn within 24 h after rest pain in patients with unstable angina and in 19 of these 26 patients in less than 6 h. In patients with unstable angina, mean +/- SD (median) values for fibrin D-dimer and plasminogen activator inhibitor values measured 0.09 +/- 0.06 (0.07) microgram/ml and 9.1 +/- 9.6 (5.9) IU, respectively, compared to 0.11 +/- 0.10 (0.05) microgram/ml and 5.5 +/- 1.9 (5.0) IU/ml, in patients in the control group (p = NS for all comparisons between the two groups). Recurrent in-hospital pain, coronary anatomy and need for intervention showed no relation to the levels of these markers. In 19 additional patients (9 with unstable angina and 10 control patients) samples from the coronary sinus and the peripheral blood were also analyzed. Again, in patients with unstable angina all samples were drawn less than 24 h after rest pain; in six of nine patients samples were drawn in less than 6 h. A coronary sinus to peripheral blood gradient for either of these markers could not be demonstrated. The differences between peripheral and coronary sinus D-dimer and plasminogen activator inhibitor concentrations were also similar in patients with unstable angina and control patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiographic patterns of balloon inflation during percutaneous transluminal coronary angioplasty: role of pressure-diameter curves in studying distensibility and elasticity of the stenotic lesion and the mechanism of dilation.

There are few in vivo data concerning the mechanisms of balloon inflation during coronary angioplasty. To characterize how lesions dilate, videodensitometry was used to measure the diameter of the inflated balloon across 29 coronary lesions in 27 patients. Pressure-diameter curves for each lesion were derived with use of a standardized incremental inflation protocol in which pressures between 2 and 6 atm in 3 mm low profile balloons approximated normal vessel diameter. The diameter of coronary stenosis before and after angioplasty was also measured. Pressure-diameter curves showed that the most improvement in luminal caliber occurred at low inflation pressure. A distensibility factor was defined as the ratio of the amount of balloon inflation at 2 atm compared with the balloon diameter at 6 atm. Eccentric irregular lesions (n = 11) had a greater distensibility factor (0.49 +/- 0.17) than did lesions (n = 18) without this configuration (0.33 +/- 0.14) (p less than 0.02). The former were soft, presumably because of thrombus in these lesions. In addition, there were no differences in patterns of balloon inflation for lesions requiring additional inflation or for dilations resulting in an intimal crack or dissection after angioplasty. There was often a loss of luminal caliber when balloon diameter at 6 atm was compared with the diameter after angioplasty. This was defined as elasticity or recoil. There was a significant direct correlation between the amount of elasticity and the extent of balloon inflation at 6 atm (that is, lesions more fully dilated at 6 atm showed more elasticity).(ABSTRACT TRUNCATED AT 250 WORDS)

Isolated chronic mitral regurgitation with preserved systolic left ventricular function and severe pulmonary hypertension.

Pulmonary hypertension in chronic mitral valve disease has been related most commonly to left ventricular dysfunction or mitral stenosis; its association with chronic, isolated mitral regurgitation and preserved left ventricular systolic function is unclear. In 41 catheterized patients with chronic mitral regurgitation (known history of mitral regurgitation for greater than 18 months) and preserved left ventricular systolic function (ejection fraction greater than 0.55), historic, electrocardiographic, echocardiographic and hemodynamic variables were analyzed. Ten patients (Group I) had normal pulmonary artery systolic pressure (less than 30 mm Hg), whereas 31 patients had pulmonary hypertension. Pulmonary artery systolic pressure was mildly increased (30 to 49 mm Hg) in 13 patients (Group II) and was greater than or equal to 50 mm Hg in 18 patients (Group III). Univariate analysis showed the more frequent occurrence of male gender and ruptured chordae tendineae in the groups with pulmonary hypertension. Mean pulmonary capillary wedge pressure, size of the V wave in pulmonary capillary wedge pressure and pulmonary arteriole resistance were higher, whereas cardiac index was lower in the hypertension groups. Multivariate stepwise analysis revealed higher mean pulmonary capillary wedge pressure and pulmonary arteriole resistance as the only variables independently differing among groups. In conclusion, pulmonary hypertension occurs frequently (76% of cases) in patients with chronic, isolated mitral regurgitation with preserved left ventricular systolic function. In these patients, a severe increase in pulmonary capillary wedge pressure is associated with elevation in pulmonary artery resistance, a finding similar to that in mitral stenosis.

Angiographic progression of coronary artery disease and the development of myocardial infarction.

There are few data on angiographic coronary artery anatomy in patients whose coronary artery disease progresses to myocardial infarction. In this retrospective analysis, progression of coronary artery disease between two cardiac catheterization procedures is described in 38 patients: 23 patients (Group I) who had a myocardial infarction between the two studies and 15 patients (Group II) who presented with one or more new total occlusions at the second study without sustaining an intervening infarction. In Group I the median percent stenosis on the initial angiogram of the artery related to the infarct at restudy was significantly less than the median percent stenosis of lesions that subsequently were the site of a new total occlusion in Group II (48 versus 73.5%, p less than 0.05). In the infarct-related artery in Group I, only 5 (22%) of 23 lesions were initially greater than 70%, whereas in Group II, 11 (61%) of 18 lesions that progressed to total occlusion were initially greater than 70% (p less than 0.01). In Group I, patients who developed a Q wave infarction had less severe narrowing at initial angiography in the subsequent infarct-related artery (34%) than did patients who developed a non-Q wave infarction (80%) (p less than 0.05). Univariate and multivariate analysis of angiographic and clinical characteristics present at initial angiography in Group I revealed proximal lesion location as the only significant predictor of evolution of lesions greater than or equal to 50% to infarction. This retrospective study suggests that myocardial infarction frequently develops from previously nonsevere lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiographic demonstration of a common link between unstable angina pectoris and non-Q-wave acute myocardial infarction.

The coronary morphology of ischemia-related arteries in unstable angina and Q-wave acute myocardial infarction (AMI) has been described. An eccentric stenosis with overhanging edges or irregular borders (type II eccentric) was seen in most lesions less than 100% occluded and probably represented plaque disruption, nonocclusive thrombus or both. The coronary morphology of non-Q AMI has not been described. Thus, the angiograms of 106 consecutive patients catheterized with either unstable angina (n = 73) or non-Q AMI (n = 33) and an identifiable ischemia-related artery were prospectively analyzed. Non-Q AMI was diagnosed by prolonged chest pain and new and persistent ST-T changes or creatine phosphokinase twice the normal level. The results showed a higher incidence of total occlusion of the ischemia-related artery in non-Q AMI (21%) compared with unstable angina (8%) (p = 0.1). The coronary morphology of nonoccluded ischemia-related arteries was similar with preponderance of type II eccentric lesions in both unstable angina and non-Q AMI. These lesions were found in 65% of ischemia-related arteries in non-Q AMI but were uncommon (3%) in nonischemia-related arteries with significant (50% to 100%) stenoses. Therefore, the type II eccentric lesion is a sensitive and specific marker of less than 100% occluded ischemia-related arteries in both unstable angina and non-Q AMI. These similarities in coronary morphology suggest a similar pathogenesis, which, as previously suggested, may relate to plaque disruption with or without thrombus. Unstable angina and non-Q AMI appear to represent part of a continuous spectrum of acute coronary artery disease. Further, the management of patients with non-Q AMI should be similar to patients with unstable angina and possibly include anticoagulation and consideration for early catheterization.

Quantitative and qualitative effects of intracoronary streptokinase in unstable angina and non-Q wave infarction.

Thrombolytic therapy has been shown to be effective in reopening totally occluded arteries in acute myocardial infarction. Coronary thrombus is also believed to play a role in the pathophysiology of unstable angina and non-Q wave infarction. However, few patients with these two acute coronary syndromes have been treated with intracoronary streptokinase. Therefore, 100,000 to 300,000 IU (mean 177,000 +/- 80,000 IU) of intracoronary streptokinase was infused into 36 consecutive catheterized patients who either presented with an acute episode of unstable angina or had had a recent non-Q wave infarction and in whom a less than 100% occluded ischemia-producing artery could be identified. Qualitative techniques utilizing vessel magnification and quantitative analysis with digital subtraction were performed on the ischemia-producing coronary lesion before and immediately after streptokinase therapy and 3 to 10 days later in 18 patients who were restudied at the time of transluminal coronary angioplasty. Before streptokinase treatment, 24 (67%) of 36 ischemia-producing arteries contained eccentric, irregular lesions. The percent diameter stenosis and percent area stenosis in all ischemia-producing arteries averaged 83.8 +/- 8.3% and 94.8 +/- 3.3%, respectively. After streptokinase treatment there were 23 arteries (64%) with eccentric irregular lesions. The percent diameter stenosis and percent area stenosis in all ischemia-producing arteries were similar to pre-streptokinase values (82.9 +/- 5.9% and 93.8 +/- 4.0%, respectively). At restudy, there were also no significant changes in any quantitative or qualitative variable. Five individual patients showed a significant reduction in percent stenosis after streptokinase. This improvement was independent of duration of symptoms, use of heparin before angiography, streptokinase dose or reduction of fibrinogen levels post-streptokinase. Two additional patients deteriorated clinically and developed total occlusion of the ischemia-producing artery within 12 hours of streptokinase infusion. These data suggest that intracoronary streptokinase may be of limited utility in either unstable angina or recent non-Q wave infarction with a less than 100% occluded ischemia-producing artery. In these syndromes, thrombus may be organized or short infusions may be given too late to be effective. In some cases, thrombus may even be absent. Whether longer infusion of streptokinase or other thrombolytic agents will be of benefit remains to be determined.