Coronary endothelial dysfunction after heart transplantation predicts allograft vasculopathy and cardiac death.

BACKGROUND: Coronary endothelial dysfunction may be an early marker for cardiac allograft vasculopathy (CAV) in orthotopic heart transplant recipients. Using serial studies with intravascular ultrasound and Doppler flow-wire measurements, we have previously demonstrated that annual decrements in coronary endothelial function are associated with progressive intimal thickening. The present study tested whether endothelial dysfunction predicts subsequent clinical events, including cardiac death and CAV development. METHODS AND RESULTS: Seventy-three patients were studied yearly beginning at transplantation until a prespecified end point was reached. End points were angiographic evidence of CAV (>50% stenosis) or cardiac death (graft failure or sudden death). At each study, coronary endothelial function was measured with intracoronary infusions of adenosine (32-microgram bolus), acetylcholine (54 microgram over 2 minutes), and nitroglycerin (200 microgram) into the left anterior descending coronary artery; intravascular ultrasound images and Doppler velocities were recorded simultaneously. Of the 73 patients studied, 14 reached an end point during the study (6 CAV and 8 deaths, including 4 with known CAV, 1 graft failure, and 3 sudden). On the last study performed, the group with an end point had decreased epicardial (constriction of 11.1+/-2.9% versus dilation of 1.7+/-2.2%, P=0.01) and microvascular (flow increase of 75+/-20% versus 149+/-16%, P=0.03) endothelium-dependent responses to acetylcholine compared with the patients who did not reach an end point. Responses to adenosine and nitroglycerin did not differ significantly. CONCLUSIONS: Endothelial dysfunction, as detected by abnormal responses to acetylcholine, preceded the development of clinical end points. These data implicate endothelial dysfunction in the development of clinically significant vasculopathy and suggest that serial studies of endothelial function have clinical utility.

Incidence and clinical significance of transient creatine kinase elevations and the diagnosis of non-Q wave myocardial infarction associated with coronary angioplasty.

To assess the incidence and clinical significance of elevated total plasma creatine kinase (CK) and MB isoenzyme fraction after apparently successful coronary angioplasty, a prospective study of 272 consecutive elective procedures was undertaken. Total CK (normal less than 100 IU/liter) and CK MB isoenzyme (normal less than 4%) were measured immediately after successful completion of the procedure and every 6 h for 24 h. All nonelective procedures and results not fulfilling all American Heart Association/American College of Cardiology Task Force guideline criteria for a successful result were excluded from analysis. Of the 272 elective procedures, 249 (92%) were successfully; abnormally elevated CK or CK MB serum levels, or both, were found in 38 (15%) of the successful outcomes. Three patterns of abnormal enzymes were identified: 15 patients with CK greater than or equal to 200 IU/liter and CK MB greater than or equal to 5% (group 1), 4 patients with CK greater than or equal to 200 IU/litter and CK MB less than or equal to 4% (group 2) and 19 patients with CK less than 200 IU/liter and CK MB greater than or equal to 5% (group 3). The three groups were distinguishable by the nature of the complications causing the enzyme release (in particular, the etiology and clinical manifestations). There were significantly more clinically apparent events in group 1 than in the other groups (13 of 15 versus 11 of 23, p less than 0.01) and more events associated with persistent electrocardiographic changes (p = 0.05) and chest pain (p less than 0.05). However, no clinically important sequelae were recognizable in any group at hospital discharge. Thus, abnormal cardiac serum enzyme release after apparently successful coronary angioplasty is 1) relatively common; 2) has many possible causes, including both minor complications and early reversibility of impending major complications; and 3) results in no permanent clinical sequelae.

Effects of previous myocardial infarction on measurements of reactive hyperemia and the coronary vascular reserve.

The measurement of coronary vascular reserve by the reactive hyperemic response to ischemia has been advocated as a practical method of assessing the physiologic significance of coronary stenoses. Because the concept of measuring coronary blood flow during maximal vasodilation assumes a normal arteriolar network and viable myocardium, the presence of previous myocardial infarction may cause a significant decrease in the coronary reserve unrelated to the severity of a coronary stenosis itself. To determine the potential importance of this effect, rest and hyperemic coronary blood flow were measured in 14 dogs in the regions subtended by the left anterior descending and left circumflex coronary arteries. One hour occlusion of the left anterior descending artery followed by reperfusion was performed in 10 dogs; the 4 remaining dogs in which no occlusion was performed served as control animals (group 3). One week later, rest and hyperemic blood flow measurements were repeated in all 14 dogs. Of the 10 dogs undergoing left anterior descending artery occlusion, 5 had a large infarct (group 1) and 5 had a small infarct (group 2). In group 1 in the 1 week study, both the coronary reserve in the left anterior descending artery zone and the ratio of the coronary reserve in this zone and the left circumflex artery zone decreased compared with values before occlusion (from 425 +/- 134 to 150 +/- 34% and from 1.56 +/- 0.40 to 0.68 +/- 0.31, respectively; both p = 0.007).(ABSTRACT TRUNCATED AT 250 WORDS)

Unstable angina and non-Q wave myocardial infarction: does the clinical diagnosis have therapeutic implications?

OBJECTIVES: The goal of this review is to reevaluate the unstable coronary syndromes in the setting of new therapies and biochemical markers. BACKGROUND: Patients with acute coronary syndromes comprise a large subset of many cardiology practices. Patients with unstable angina (UA) and non-Q wave myocardial infarction (NQMI) may sustain a small amount of myocardial loss but have significant amounts of viable, yet ischemic, myocardium, placing them at high risk for future cardiac events. In the past, enzyme differentiation of NQMI from UA was considered important to assess prognosis and direct therapy. METHODS: Manuscripts published in peer-reviewed journals over the past three decades were reviewed and selected for this review. Recent abstracts were also considered and cited where appropriate. RESULTS: In the late 1990's, although UA and NQMI remain parts of a spectrum, it is apparent that the distinction between these two entities is no longer sufficient to identify high risk patients; rather, specific electrocardiographic changes, aspects of the clinical history, newer biochemical markers, and angiographic findings help to better distinguish higher risk individuals from a large patient population with unstable coronary syndromes and these factors usually determine therapy. CONCLUSIONS: Based on these results, it is likely that newer therapies such as glycoprotein IIb/IIIa receptor antagonists, low molecular weight heparins, and coronary stents will be directed toward these high risk patients.

Acute coronary hemodynamic response to cigarette smoking in patients with coronary artery disease.

The acute changes in coronary blood flow and coronary resistance that occur in response to cigarette smoking have not been accurately determined. To define the factors that affect this response, coronary sinus blood flow was measured in 16 patients (group I) with coronary artery disease and in 6 patients (group II) without angiographically detectable coronary disease. Seven patients (group IA) had severe (greater than or equal to 75%) proximal left coronary lesions and nine patients (group IB) had significant distal lesions with 50% or less proximal stenoses. Group I had a smaller overall increase (increases 1.6 +/- 5.3%) in coronary sinus blood flow than did group II (increases 7.7 +/- 6.1%) (p less than 0.05). Coronary resistance increased overall (increases 2.7 +/- 5.3%) in group I but decreased (decreases 2.4 +/- 3.4%) in group II (p less than 0.05). Patients in group IA had a highly significant increase in coronary resistance as compared with group IB (increases 7.0 +/- 4.2% versus decreases 0.9 +/- 2.6%) (p less than 0.001). Coronary sinus flow tended to decrease (decreases 1.2 +/- 4.6%) in group IA but to increase (increases 3.8 +/- 5.1%) in group IB (p = 0.06). It is concluded that smoking increases coronary resistance in patients with coronary artery disease. A greater impact is observed in patients with a severe proximal stenosis than in those with a distal stenosis. It is proposed that smoking increases coronary artery tone at the site of the stenosis, limiting the coronary flow response proportionally to the size of the affected vascular bed.

Validated risk stratification model accurately predicts low risk in patients with unstable angina.

BACKGROUND: In the mid 1990s, two unstable angina risk prediction models were proposed but neither has been validated on separate population or compared. OBJECTIVES: The purpose of this study was to compare patient outcome among high, medium and low risk unstable angina patients defined by the Agency for Health Care Policy and Research (AHCPR) guideline to similar risk groups defined by a validated model from our institution (RUSH). METHODS: Four hundred sixteen patients consecutively admitted to the hospital with unstable angina between January 1, 1995, and December 31, 1997, were prospectively evaluated for risk factors. The presence of major adverse events such as myocardial infarction (MI), death and heart failure was assessed for each patient by chart review. RESULTS: The composite end point of heart failure, MI or death occurred in 3% and 5% of the RUSH and AHCPR low risk categories, respectively, and in 8% and 10% of AHCPR and RUSH high risk categories, respectively. Recurrent ischemic events were best predicted by the RUSH model (high: 24% vs. medium: 12% and low: 10%, p = 0.029), but not by the AHCPR model (high: 14% vs. medium: 13% and low: 9%, p = 0.876). The RUSH model identified five times more low risk patients than the AHCPR model. CONCLUSIONS: Both models identify patients with low and high event rates of MI, death or heart failure. However, the RUSH model allowed for five times more patients to be candidates for outpatient evaluation (low risk) with a similar observed event rate to the AHCPR model; also, the RUSH model more successfully predicted ischemic complications. We conclude that the RUSH model can be used clinically to identify patients for early noninvasive evaluation, thereby improving cost effectiveness of care.

Effects of chronic tobacco smoking on the coronary circulation.

The effects of chronic smoking on the coronary circulation were studied by evaluating the coronary vascular reserve in 12 chronic smokers (group 1) and 10 nonsmokers (group 2). All patients were referred to cardiac catheterization for evaluation of chest pain and were found to have normal coronary and left ventricular angiograms. Coronary vascular reserve was measured by analyzing the hyperemic response to selective coronary injection of contrast agent. There was no statistically significant difference between groups 1 and 2 with regard to age, baseline electrocardiogram or response to treadmill or thallium-201 exercise tests. The mean coronary reserve (+/- standard deviation) was 74.1 +/- 20.1% in the smokers versus 117.1 +/- 45.1% in the nonsmokers (p less than 0.02). In patients who smoked 1 pack a day or less and in those who smoked more than 1 pack a day, the mean coronary reserve was 89.5 and 64.9%, respectively (p less than 0.05). Additionally, of 20 patients followed up for an average of 20 months, 7 of 10 smokers and 1 of 10 nonsmokers continued to have chest pain (p less than 0.03). The cause for the chest pain has not been established in these patients. These results suggest that coronary vascular reserve is significantly less in chronic smokers than in nonsmokers, and that this decrease is more pronounced in heavy smokers.

Clinical practice guidelines in unstable angina improve clinical outcomes by assuring early intensive medical treatment.

OBJECTIVES: To determine the influence of clinical practice guidelines on treatment patterns and clinical outcomes in unstable angina and the effectiveness of guideline reminders on implementing practice guidelines, two groups of medium and high risk patients with unstable angina were compared. BACKGROUND: New guidelines have been published by the Agency for Health Care Policy and Research (AHCPR) for evaluating and managing patients with unstable angina. The impact of these guidelines to improve the quality of care has never been tested. METHODS: Group 1 included 338 consecutive medium or high risk patients admitted before publication of the AHCPR guidelines, and group 2 consisted of 181 consecutive similar risk patients admitted after institution of the AHCPR guideline reminders at this institution. Dissemination of clinical practice guidelines was ensured by a grand rounds lecture and by posting guideline reminders on all group 2 patients' charts within 24 h of admission. RESULTS: The two groups were similar in terms of most baseline characteristics, including hypercholesterolemia, diabetes, hypertension, smoking history, baseline ST segment depression and previous coronary artery bypass graft surgery. Group 1 patients were older (68+/-13 vs. 63+/-16 years, p = 0.001) and more frequently had a previous myocardial infarction (39% vs. 22%, p = 0.001). Group 2 patients more frequently required intravenous nitroglycerin to control the index episode of chest pain (43% vs. 34%, p = 0.003). Group 2 patients more frequently received aspirin (96% vs. 88%, p = 0.009) during admission and underwent coronary angiography (71% vs. 58%, p = 0.006). More importantly, group 2 patients received oral beta-blockers (p = 0.008), aspirin and coronary angiography (p = 0.001) earlier than group 1 patients and experienced recurrent angina (29% vs. 54%) and myocardial infarction or death less frequently (3% vs. 9%, p = 0.028). CONCLUSIONS: In unstable angina, clinical practice guidelines were associated with greater use of aspirin and coronary angiography and greater use and earlier administration of beta-blockers. Variation in drug use over time was also reduced. Objective improvement in clinical outcome was also noted. Thus, practice guidelines improve the quality of care of patients with unstable angina.

Does low individual operator coronary interventional procedural volume correlate with worse institutional procedural outcome?

OBJECTIVES: To assess the relation between individual operator coronary interventional volume and incidence of complications, the in-hospital outcome at a single, moderate volume urban academic center was prospectively collected over a 3-year period. BACKGROUND: A minimum of 75 coronary interventions/operator per year may be required in the future to obtain formal certification. However, few data exist regarding individual operator volumes and procedural outcome. METHODS: Between January 1993 and December 1995, 1,389 consecutive procedures were performed or supervised by nine geographic full-time operators: 171 (12.3%) utilized various devices, and 350 (25.2%) involved multivessel coronary intervention. Left ventricular ejection fraction was 59 +/- 15% (mean +/- SD), and there were 1.7 +/- 0.7 vessels diseased (with > or = 70% stenosis). Clinical indications included stable angina in 22.5% of cases, unstable angina in 31.9%, acute myocardial infarction (MI) in 2.9%, post MI in 20.6%, shock or acute heart failure in 3.0% and restenosis in 19.1%. In the last consecutive 857 lesions in 655 cases, 20.7% type A, 55.5% type B and 23.8% type C lesions were categorized before coronary intervention. RESULTS: Average yearly operator volume ranged from 26 to 83 cases (mean 51 +/- 26). Each operator has performed a total of 590 +/- 268 coronary interventions, with 10.0 +/- 4.3 years of coronary interventional experience. The mean angioplasty volume rating for the nine operators was 180 +/- 37 (> 170 considered adequate). The in-hospital major complication rate was 1.4% (95% confidence interval 0.7% to 1.893%) for all coronary interventions, including death in 3 patients, bypass surgery in 13, arrhythmia in 3 and Q wave MI in 2. To ascertain how these outcomes compared with standard measures of coronary interventional outcome, four previously published registries were reanalyzed in a similar manner. The rate of complications in the present study was found to be significantly lower than that of the 1992-1993 Society for Cardiac Angiography and Intervention registry (1.9%, n = 19,594, p < 0.05 [excludes ventricular arrhythmias]), the 1994 American College of Cardiology database (3.9%, n = 38,963, p = 0.001), the Mid-America Heart Institute outcome in 1988 (2.3%, n = 5,413, p = 0.02) and the 1985-1986 National Heart, Lung, and Blood Institute Registry (7.2%, n = 1,801, p = 0.001). Odds ratios and 95% confidence intervals showed the outcome in the current study to be at least comparable to the standard registries. CONCLUSIONS: Despite individual operator volumes below those currently being considered for credentialing, the overall institutional outcome was excellent in a diverse and complex patient population.

Absence of coronary vascular reserve in myocardium distal to a fixed coronary stenosis.

In a study to test the hypothesis that vascular reserve is exhausted in the setting of a resting blood flow deficit, the left anterior descending or circumflex artery was cannulated and perfused from the left carotid artery. After reactive hyperaemia had been assessed a stenosis was produced with a screw clamp. In the first experiment a moderate stenosis (diastolic perfusion pressure 40 mmHg) was produced in the left anterior descending artery (three dogs) or left circumflex artery (three dogs). Blood pressure was held constant with aortic constriction during intracoronary adenosine infusion (6 mumol.min-1). The stenosis was then adjusted to the preadenosine perfusion pressure. In the second experiment the anterior interventricular coronary vein was also isolated and segment length crystals were placed in the ischaemic and non-ischaemic zones. Severe stenosis (flow reduction of at least 50% and evidence of decreased segmental shortening) was produced in the cannulated left anterior descending artery (eight dogs). Intracoronary adenosine was given with aortic pressure held constant by transfusion and coronary venous drainage. In the first experiment resting coronary flow (ml.min-1) decreased from 41(3) to 29(6) (p less than 0.05) with stenosis. Coronary flow increased from 29(6) to 34(7) (p less than 0.05) with adenosine and to 50(10) (p less than 0.05) with stenosis adjustment. Subendocardial flow (ml.g-1.min-1) decreased from 0.89(0.26) to 0.78(0.23) (p less than 0.05) with adenosine and then increased from 0.94(0.49) with perfusion pressure adjustment. Subepicardial flow tended to increase with adenosine, and increased further with stenosis adjustment.(ABSTRACT TRUNCATED AT 250 WORDS)

Contractile function and reserve during acute ischaemia in the canine lateral border zone.

The hypothesis that there is a lateral border zone with function intermediate to adjacent ischaemic and non-ischaemic tissue was tested in 10 open chest anaesthetised dogs. Four pairs of segment length crystals were placed in parallel so as to span the ischaemic and non-ischaemic zones. Graded occlusion was produced with a screw clamp applied to a carotid to left anterior descending artery cannulation system. Contractile reserve was assessed using postextrasystolic potentiation. A balloon perfusion labelling system was used to label negatively the potentially ischaemic zone and quantify the admixture of ischaemic and non-ischaemic tissue in the lateral border zone, defined by the fraction of normal zone tissue. When the 40 crystal pairs from the 10 dogs were grouped according to fraction of normal zone tissue (FNZT), 13 were in the central ischaemic zone (FNZT less than 0.1), seven were in the border ischaemic zone (FNZT 0.1-0.5), five were in the border non-ischaemic zone (FNZT 0.5-1.0), and 15 were in the non-ischaemic zone (FNZT 1.0). When the lateral border zone is predominantly non-ischaemic tissue, the tissue behaves as though it is non-ischaemic. Segmental shortening before and after postextrasystolic potentiation in the border non-ischaemic zone and non-ischaemic zone did not change with ischaemia. When tissue in the lateral border zone is predominantly ischaemic, it behaves as though it is ischaemic. Segmental shortening decreased in parallel with progressive ischaemia in the border ischaemic zone and ischaemic zone. At total occlusion, segmental shortening in the border ischaemic zone was -2.3(5.9%) and in the ischaemic zone -3.5(3.6)% (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

A non-linear elastic model of contraction of ischaemic segments.

Previous studies have characterised the motion of the myocardium using a linear time varying elastance model, ie, they have sought to characterise the relationship between left ventricular volume and internal pressure as linear, but with time varying slopes over the cardiac cycle. However, the motion of myocardium during regional ischaemia has not been characterized by such models. Studies of totally ischaemic tissue and of myocardium in diastole have characterised the relationship between tension or stress and segment length as exponential. It is the purpose of this study to present a new model in which myocardial contraction is expressed as an exponential, but time varying elastic relationship. In this model tension, T, is related to segment length according to the formula T = e alpha(t)L + beta, where alpha(t) rises with systole and falls in diastole. This model was applied to the motion of hypokinetic segments noted in a series of conscious dogs studied for other purposes. Hypokinetic segments display early systolic bulging, decreased systolic shortening, and early diastolic recoil. These particular types of segment motion are naturally predicted by this model. Furthermore, the motion of myocardial segments as they become increasingly ischaemic may be predicted, including a gradual shift to the right and narrowing of the tension-length loop. alpha was noted to be independent of loading change, and thus may be viewed as an index of contractility. This model thus predicts the pattern of motion of hypokinetic segments and provides new insight into myocardial contractility.

Improved survival with coronary bypass surgery in patients with three-vessel coronary disease and abnormal left ventricular function. Matched case-control study in patients with potentially operable disease.

Recent studies have suggested that patients with three-vessel coronary disease and abnormal left ventricular function have better survival rates with bypass surgery than with medical therapy alone. Case-control studies may give accurate survival estimates, but to be valid, selection biases must be taken into account. A matched case-control method was used to compare survival patterns in patients treated medically or surgically during the 1980s. Fifty medical patients with potentially operable coronary disease and 46 surgical patients were matched for significant three-vessel disease and abnormal ventricular function. These two groups had no significant differences with regard to 24 variables, including age (64 +/- 8 versus 63 +/- 10 years), chest pain class, congestive heart failure signs, ejection fraction (36 +/- 8 versus 37 +/- 9 percent), segmental wall score, or a coronary score evaluating lesion site and severity. There were slight differences between the two groups with regard to congestive heart failure symptoms (p = 0.04). Patients undergoing bypass surgery had improved four-year survival rates compared with the medical group (89 versus 55 percent; p = 0.01). Thus, this study used an effective case-control method to suggest that, in the 1980s, coronary surgery improves prognosis substantially in surgically approachable patients with severe coronary disease and ventricular dysfunction.

Comparison of heparin therapy for < or = 48 hours to > 48 hours in unstable angina pectoris.

Of 450 consecutive patients with unstable angina admitted to a tertiary care, university-based medical center over a 24-month period, 334 were administered heparin and aspirin for some length of time. Two groups of 98 patients matched for acuity and gender at baseline were treated with either < or = 48 hours (group 1) or > 48 hours (group 2) of heparin. The acuity model used in this study incorporates 6 factors: age, recent myocardial infarction, treatment with intravenous nitroglycerin, previous therapy with beta blockers or calcium antagonists, baseline ST depression, and diabetes. Despite similar risks and overall clinical outcome, group 2 had significantly more myocardial infarction or death after 48 hours than group 1 (p = 0.01). In part, this was due to a delay in the performance of coronary angiography (2.8 +/- 1.4 vs 3.5 +/- 15 days, p = 0.01), coronary intervention (2.7 +/- 1.8 vs 5.1 +/- 2.3 days, p = 0.01), and bypass surgery (3.8 +/- 3.6 vs 7.0 +/- 5.6 days, p = 0.02). There was no difference between groups regarding the success of coronary intervention (90% vs 88%, p = NS). Heparin duration was influenced by the finding of intracoronary thrombus or ulceration on angiography before revascularization, as each finding was seen more often in group 2 (thrombus, 12% vs 24%; ulceration, 38% vs 60%). These results suggest that the optimal duration of heparin therapy is up to 48 hours after admission in unstable angina; a longer time period is associated with increased adverse consequences.

Importance of total life consumption of cigarettes as a risk factor for coronary artery disease.

Cigarette smoking is an established risk factor for the occurrence of cardiovascular events and mortality. Whether recent smoking history or total life consumption best represents the increased risk due to smoking has not been previously established. Thus, stepwise logistic regression analysis was used to determine the relative contributions of these factors to the risk of having significant coronary artery disease in 1,349 patients who underwent cardiac catheterization. Six risk factors were analyzed: total pack-years, current packs smoked per day, age, gender, family history and symptomatic status. The results of this analysis showed that total pack-years, but not current packs per day, is a significant independent risk factor for the development of coronary artery disease. This was true in every age group up to but not older than age 70 years. Although the overall risk was lower in younger patients and in patients with less typical symptoms of angina, the relative risk in cigarette smokers relative to pack-years was consistently greater. The risk of total life consumption of cigarettes is thus greater than has heretofore been realized, particularly in persons who would otherwise be categorized as low risk.

Prognosis of symptomatic coronary artery disease in young adults aged 40 years or less.

The clinical course and coronary angiographic features of symptomatic coronary artery disease (CAD) in patients younger than 40 years old are described with particular emphasis on the prevalence of myocardial infarction and the degree of diminished functional capacity. Eighty-five patients with CAD proven by coronary angiography were studied. There were 73 men and 12 women aged 27 to 40 years. Fifty-nine patients presented with acute myocardial infarction, most of whom denied previous chest pain, and 14% (12 patients) presented with less acute chest pain syndromes. Coronary angiography was performed in all patients, and greater than or equal to 70% luminal diameter narrowing was considered significant. Coronary angiographic findings reveal 51% with 1-vessel CAD, 31% with 2-vessel and 19% with 3-vessel. Subsequently, 23 patients had coronary artery bypass graft surgery, 7 underwent angioplasty and 55 were treated medically. Follow-up for a mean of 3 years revealed only 1 death and 4 subsequent hospital admissions for cardiac events. Fifty-three percent of the patients are entirely pain free, and only 4 (5%) have significant symptoms of angina pectoris. Although 15 (18%) are not employed regularly, the remainder work full- or part-time, or plan to work in the near future. These data suggest that the short-term prognosis and functional status of young patients with CAD is excellent.

Balloon dilatation of symptomatic subacute intimal dissection presenting as restenosis.

Repeat percutaneous transluminal coronary angioplasty (PTCA) for subacute intimal dissections that produce symptoms after a period of 1 month or more is reluctantly performed for fear of extension and abrupt closure. Patients were identified with demonstrated intimal dissections (intimal contrast staining or frank intimal flap) at the time of initial PTCA who returned a mean of 17.5 weeks (range 9 to 50) later with recurrent chest pain. Repeat angiography revealed luminal compromise due to dissection rather than restenosis in 22 patients. Of these, 17 underwent repeat PTCA. Elective bypass surgery without attempted PTCA was chosen in the other 5 patients because of extensive intimal dissections (greater than 2 balloon lengths) or involvement of critical branches. In the group of 17 patients who had repeat PTCA, 10 (group 1) had a frank intimal flap without persistent contrast staining after the initial PTCA, while 7 (group 2) had both persistent staining and a flap. Successful PTCA was performed in 13 of these 17 patients (76%). There were 2 abrupt closures and 2 unsatisfactory luminal openings. One of these patients required urgent coronary bypass surgery. All 10 group 1 patients had successful repeat procedures versus only 3 of 7 group 2 patients (p = 0.01). The 3 patients with the greatest degree of luminal compromise immediately after the initial PTCA had failed repeat PTCA attempts. These results suggest that repeat PTCA for subacute intimal dissections presenting as restenosis can be successfully performed in selected patients, and that the presence of contrast staining and the degree of luminal compromise by the dissection may be predictive of outcome.

Utility of various clinical, noninvasive, and invasive procedures for determining the causes of recurrence of myocardial ischemia or infarction > or = 1 year after percutaneous transluminal coronary angioplasty.

In patients with recurrent symptoms > or = 1 year after successful percutaneous transluminal coronary angioplasty (PTCA), the decision of whether to proceed directly with coronary angiography or to evaluate the patient noninvasively can be difficult. To determine which demographic, historical, clinical, and laboratory factors are useful in helping to make this decision, 76 consecutive patients who presented > 1 year (768 +/- 309 days) after successful PTCA with resolution of symptoms were studied. The initial PTCA successfully treated all stenoses (except chronically occluded vessels) in all major vessels and segments. The patient group was predominantly men (68%), with a mean age of 64 +/- 10 years. A prior myocardial infarction was present in 39 patients (51%), and there was a mean of 2.8 risk factors per patient. In patients who presented with recurrent symptoms, the Canadian Cardiovascular Society functional class was 2.0 +/- 0.9; 2 patients presented with acute infarctions, 57 were admitted to the hospital with unstable angina, and 17 had stable angina. New electrocardiographic changes at rest were found in 19 of 74 patients (26%) with recurrent angina. A thallium stress test was performed in 40 patients (53%), with a sensitivity of 77% and a specificity of 36% for the presence of a significant stenosis. No nonangiographic variable was predictive of angiographic findings. At angiography, the number of coronary arteries with > or = 50% diameter narrowing was 1.4 +/- 1.0. Forty-two patients had stenosis at a new site, 7 had restenosis, and 27 had no new stenoses.(ABSTRACT TRUNCATED AT 250 WORDS)

Medical and surgical survival in coronary artery disease in the 1980s.

The survival of 1,657 patients with angiographically proved coronary artery disease (CAD) was studied for 4 years (mean 2.0 +/- 1.2) during the 1980s to examine the prognostic importance of multiple clinical variables. One hundred of the 1,049 medically treated patients (9.5%) and 31 of the 608 surgically treated patients (5.1%) died. Multivariate analyses revealed that the strongest prognostic variables for survival in the medical group were indexes of left ventricular function (p less than 0.0001), severity of coronary stenoses (p less than 0.0001) and age (p = 0.005). However, only age (p less than 0.0001) was a significant prognostic variable in the surgically treated group. This study emphasizes the lack of prognostic significance of left ventricular function indexes and severity of coronary stenoses in surgically treated patients with CAD. These results continue the trend toward improved surgical survival shown in recent years.

Multistage analysis of exercise radionuclide angiography in coronary artery disease.

The hypothesis that serial assessment of left ventricular function during exercise radionuclide angiography provides improved diagnostic criteria for coronary artery disease (CAD) was examined. Fifty-eight consecutive patients without previous myocardial infarction were prospectively scheduled for cardiac catheterization and multistage radionuclide angiographic exercise studies. Forty-one patients had significant CAD. The traditional criterion--failure to achieve a 5% increment in ejection fraction (EF) during exercise compared with the value at rest--had 85% sensitivity but only 41% specificity for CAD. In 12 patients, EF increased early in exercise by at least 4% and then decreased a mean of 7.5%, often with worsening regional wall motion. This "up-down" EF pattern was applied as a diagnostic test in the overall study group. Analysis of changes in EF from the maximal value achieved to that at the end of exercise resulted in criteria with greater sensitivity (p less than 0.0001) for CAD than analysis of changes from rest, with similar specificity. Regional wall motion abnormalities occurring during the first exercise stage resulted in 94% specificity for CAD (p = 0.05 vs end-stage analysis), although sensitivity was low. Analyzing the maximal EF during exercise results in improved sensitivity, while analyzing the early onset of regional dysfunction results in high specificity for CAD.