Mark Warner

Frequency of coronary artery disease and left ventricular dysfunction in cocaine users

To evaluate the spectrum of coronary artery disease (CAD) in cocaine users, coronary angiograms obtained from 33 patients (26 men [79%] and 7 women [21%], mean age 37 years) with history of cocaine use and cardiac symptoms were retrospectively reviewed. Clinical indications for coronary angiograms included chest pain (n = 28), congestive failure (n = 4) and complete heart block (n = 1). Coronary angiograms were reviewed independently by 2 angiographers unaware of patients clinical status. Thirteen patients (40%) had normal coronary angiograms, and 20 (60%) had CAD; 7 (21%) had mild CAD (less than or equal to 70% diameter stenosis), and 13 (40%) had significant CAD (greater than 70% diameter stenosis). Of 13 patients with significant CAD, 7 had 1-vessel, 4 had 2-vessel and 2 had 3-vessel CAD. There was enzymatic evidence of myocardial infarction in 12 of 33 patients (36%); all 12 had CAD (10 with significant and 2 with mild CAD). Mean age and number of risk factors (serum total cholesterol, cigarette smoking, systemic hypertension, diabetes mellitus, family history of CAD, and obesity) in patients with CAD (mild or significant) and with normal coronary angiograms were not statistically different. Left ventricular ejection fraction was normal in 15 patients (45%) and depressed in 18 (55%). All patients with CAD and low ejection fractions (n = 12) had regional wall motion abnormalities, whereas all those with normal coronary arteries and low ejection fraction (n = 6) had global hypokinesia.

Intracoronary urokinase as an adjunct to percutaneous transluminal coronary angioplasty in patients with complex coronary narrowings or angioplasty-induced complications

The effectiveness of intracoronary urokinase infusion as an adjunct to percutaneous transluminal coronary angioplasty (PTCA) was studied in 50 patients who underwent angioplasty for complex coronary narrowings or had thromboembolic complications during PTCA (29 [58%] men, 3 [6%] stable and 37 [74%] unstable angina, and 16 [32%] prior coronary bypass surgery). The primary indications for intracoronary urokinase infusion were intracoronary thrombus in 27 patients (54%), distal coronary embolization in 9 (18%), and abrupt reclosure in 14 (28%). Urokinase was infused in a mean (+/- standard deviation) dosage of 399,000 +/- 194,000 IU (range 150,000 to 1,000,000) at an average rate of 5,000 to 20,000 IU/min. Angiographic success was achieved in 43 patients (86%). Complications included the need for urgent bypass surgery in 3 patients, Q-wave myocardial infarction in 2, and non-Q-wave myocardial infarction in 12 (8 of whom had peak creatine kinase less than twice the upper normal limit). The incidence of myocardial infarction was significantly higher in patients with vein grafts (69%) than in those with PTCA of native vessels (14%). Two patients died (1 massive gastrointestinal necrosis 24 hours after angioplasty, and 1 after urgent bypass surgery). Mean (+/- standard deviation) fibrinogen levels were 355 +/- 73 mg/dl before urokinase infusion, and 361 +/- 70, twelve hours afterward. Three patients had local bleeding, but no transfusions were needed. It is concluded that intracoronary urokinase is a safe and effective adjunct to PTCA in patients with associated thrombi and may improve the success rate in angioplasty complicated by thrombus formation.

Complete left main coronary artery occlusion: angiographic evaluation of collateral vessel patterns and assessment of hemodynamic correlates.

An angiographic study of eight patients with total occlusion of the left main coronary artery identified six patients with chronic occlusion and two with acute complete occlusion. In each of six patients, there were two to six different intercoronary collateral pathways. Altogether, a total of 13 specific collateral channels were recognized. One patient had evidence of unique homocollaterals represented by enlarged vasa vasorum, which created a vascular cuff that surrounded a totally obstructed left main artery. The ventricular function and hemodynamic parameters in these patients not only depend on the collateral vessels but may also be affected by the severity of coronary artery disease in the artery that supplies collaterals.

Absent left main coronary artery: Angiographic findings in 83 patients with separate ostia of the left anterior descending and circumflex arteries at the left aortic sinus

Among 20,332 adult patients who underwent consecutive cardiac catheterization and coronary arteriography, 83 (0.4%) were angiographically identified as having an absent left main coronary artery. The angiographic characteristics of this coronary anomaly include: (1) the presence of two well-separated coronary ostia at the left aortic sinus resulting in separate origin of the left anterior descending and circumflex arteries; (2) an increased incidence of left coronary dominance; (3) a higher (6%) than usual (0.5% to 1.5%) incidence of myocardial bridging; (4) lack of a high incidence of congenital heart anomalies; and (5) an incidence of atherosclerotic coronary artery disease similar to that of patients whose left main artery is intact. In 39% of the patients difficulties in selectively cannulating the separate ostium of the circumflex artery and adequately opacifying this vessel resulted in a need to change the diagnostic catheter size. Recognition of this coronary anomaly is needed to ensure accurate angiographic interpretation and is important for patients undergoing cardiac surgery to selectively perfuse these separate vessels during cardiopulmonary bypass.

Immediate and long-term results of delayed recanalization of occluded acute myocardial infarction-related arteries using coronary angioplasty

Recent evidence suggests that late reperfusion of an occluded infarct-related artery after acute myocardial infarction (AMI) may convey a better prognosis. The clinical outcome of percutaneous transluminal coronary angioplasty (PTCA) as a means of mechanical reperfusion in this particular setting has not been clearly delineated. Ninety-seven patients with AMI underwent PTCA of the occluded infarct-related artery after the acute phase of the AMI (48 hours to 2 weeks, mean 8 +/- 4 days). The study consisted of 72 men (74%) (mean age 56.5 +/- 12 years) and 25 women. Seventy-seven patients (79%) had a Q-wave AMI and 20 patients (21%) a non-Q-wave AMI. Seventy-six patients (79%) had angina after AMI and 4 had previously undergone coronary bypass surgery. Clinical success was achieved in 85 patients (87%). Angiographic success was obtained in 90 of the 97 occluded arteries (93%) and was similar for all 3 major vessels: right coronary 97%, left anterior descending 93% and circumflex 85% (p = not significant). Major complications (AMI, emergency bypass and death) occurred in 3 patients (3.1%). Long-term follow up (3.7 +/- 0.8 years) revealed symptomatic recurrence in 20 (23%), whereas 51 (58%) remained asymptomatic. Most recurrences (16 of 20) were in the form of restenosis rather than reocclusion, with a high success rate for repeat dilation (93%). These results indicate that mechanical reperfusion of an occluded infarct artery, performing PTCA 48 hours to 2 weeks after AMI, has a high success rate, a low complication rate and low symptomatic restenosis.

Long-term efficacy of triple-vessel angioplasty in patients with severe three-vessel coronary artery disease.

Between May 1982 and December 1988, a total of 103 patients underwent angioplasty of all three major coronary arteries at a single institution. Angiographic success was achieved in 334 of 352 vessels (95%) and in 441 of 460 lesions (96%). No patients required urgent bypass surgery, and none died during the procedure; six had non-Q wave infarctions. The mean length of follow-up time was 49 +/- 15 months (range 28 to 107 months). There have been 11 deaths, and one patient has undergone cardiac transplantation. Thirty-six patients had a clinical recurrence; 30 had repeat angioplasty and five had bypass surgery. Another nine patients eventually had bypass surgery after the clinical recurrence. At 48 months actuarial event-free rates are myocardial infarction, 98%; bypass surgery, 88%; and death, 89%. Of 86 current survivors, 58 are in functional class O to I, 21 are in class II, and seven are in class III.

Mechanical and subcellular function of the canine heterotopic transplanted myocardium during active transplant injury.

A chronically instrumented canine cardiac allograft has been developed to follow sequential mechanical, electrical, and subcellular function. In the first group (n = 6), base line mechanical activity (dP/dt-max) demonstrated a period of recovery from 48 to 72 hr (control = 2200 ± 100 mm Hg/sec; group 1 = 2800 ± 100 mm Hg/sec, P < 0.05), followed by the onset of immune injury and increasing depression of function until day 8 (1000 ± 100 mm Hg/sec). Maximal activation (0.25 μg of adrenalin/kg of recipient weight) was 3800 ± 200 mm Hg/sec at day 1 and progressively decayed through day 8 (1900 ± 100 mm Hg/sec, P < 0.01). The chronotropic response to maximal activation (MA) remained intact until day 7 (control = 121 ± 9 beats/min; MA = 188 ± 6 beats/min, P < 0.01). In a second series, mechanical activity and the function of the isolated sarcoplasmic reticulum (SR) and myofibrils were studied in a 24-hr post-transplant group (T + 24, n = 6) and a 3− to 4-day post-transplant group (T + 72, n = 6). In the absence of MA, neither positive nor negative dJP/dt-max was significantly different in the two groups. With MA, positive and negative dP/dt-max decreased significantly in the T+ 72 animals (+dP/dt-max: T + 24 = 6600 ± 100, T + 72 = 3500±100 mm Hg/sec, P < 0.05; -dP/dt-max: T + 24 = 5900 ± 60, T + 72 = 2800 ± 60 mm Hg/sec, P < 0.05). Left ventricular biopsies of the 3− to 4-day post-transplant group showed acute immune injury. Myofibrillar function, as assessed by pCa-ATPase curves, was depressed when compared to nontransplanted (C, n = 4) myofibrillar activity. Vmax at pCa = 5.4: C = 0.180 ± 0.005; T + 24 = 0.060 ± 0.005; T + 72 = 0.108 ± 0.005 μmol Pi/mg-min. The Vmax of the 3− to 4-day post-transplant group was significantly greater than the controls. Oxalate supported calcium transport by the isolated SR from both the T + 24 and T + 72 group was significantly depressed (C = 0.92 ± 0.05; T + 24 = 0.22 ± 0.02; T + 72 = 0.20 ± 0.02 μmol Ca2+/mg-min; P < 0.01). Ca2+-stimulated, Mg2+-dependent ATPase activity of the SR isolated from the T + 24 group demonstrated uncoupling of ATP hydrolysis from calcium transport (C = 1.15 ± 0.100, T + 24 = 0.75 ± 0.100 μmol Pi/mg-min), while the T + 72 group demonstrated a significant depression of SR ATPase activity (0.30 ± 0.05 μmol Pi/mg-min, P < 0.01). The SR coupling ratio (Ca2+ transported/Pi hydrolysis) confirmed uncoupling in the T + 24 group (C = 0.875, T + 24 = 0.275) and depression in the 3− to 4-day post-transplant group (T + 72 = 0.796). Transplant injury is multifactorial with an initial phase of ischemia-reperfusion injury with the maintenance of normal mechanical function but a significant depression in activity of the isolated SR and myofibrils. With the onset of immune injury, there is a depression of mechanical function as well as a depression of both myofibrillar ATPase function and SR calcium transport and ATPase activity.