Harry R. Phillips

Prognostic value of a coronary artery jeopardy score

The prognostic value of a coronary artery jeopardy score was evaluated in 462 consecutive nonsurgically treated patients with significant coronary artery disease, but without significant left main coronary stenosis. The jeopardy score is a simple method for estimating the amount of myocardium at risk on the basis of the particular location of coronary artery stenoses. In patients with a previous myocardial infarction, higher jeopardy scores were associated with a lower left ventricular ejection fraction. When the jeopardy score and the number of diseased vessels were considered individually, each descriptor effectively stratified prognosis. Five year survival was 97% in patients with a jeopardy score of 2 and 95, 85, 78, 75 and 56%, respectively, for patients with a jeopardy score of 4, 6, 8, 10 and 12. In multivariable analysis when only jeopardy score and number of diseased vessels were considered, the jeopardy score contained all of the prognostic information. Thus, the number of diseased vessels added no prognostic information to the jeopardy score. The left ventricular ejection fraction was more closely related to prognosis than was the jeopardy score. When other anatomic factors were examined, the degree of stenosis of each vessel, particularly the left anterior descending coronary artery, was found to add prognostic information to the jeopardy score. Thus, the jeopardy score is a simple method for describing the coronary anatomy. It provides more prognostic information than the number of diseased coronary arteries, but it can be improved by including the degree of stenosis of each vessel and giving additional weight to disease of the left anterior descending coronary artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of a QRS scoring system for estimating myocardial infarct size

This study correlated the location and size of posterolateral myocardial infarcts (MIs) measured anatomically with that estimated by quantitative criteria derived from the standard 12-lead ECG. Twenty patients were studied who had autopsy-proved, single, posterolateral MIs and no confounding factors of ventricular hypertrophy or bundle branch block in their ECG. Left ventricular anatomic MI size ranged from 1 to 46%. No patient had a greater than or equal to 0.04-second Q wave in any electrocardiographic lead and only 55% had a 0.03-second Q wave. A 29-point, simplified QRS scoring system consisting of 37 weighted criteria was applied to the ECG. Points were scored by the ECG in 85% of the patients (range 1 to 8 points). MI was indicated by a wide variety of QRS criteria; 19 of the 37 criteria from 8 different electrocardiographic leads were met. The correlation coefficient between MI size measured anatomically and that estimated by the QRS score was 0.72. Each point represented approximately 4% MI of the left ventricular wall.

Evaluation of a QRS scoring system for estimating myocardial infarct size. II. Correlation with quantitative anatomic findings for anterior infarcts

The ability of an independently developed QRS point score to estimate the size of infarcts predominantly within the anterior third of the left ventricular was evaluated by quantitative pathologic-electrocardiographic correlation. The study was limited to 21 patients with a single infarct documented by postmortem examination, for whom an appropriately timed standard 12 lead electrocardiogram was available that did not exhibit signs of left or right ventricular hypertrophy, left or right bundle branch block or anterior or posterior fascicular block. At necropsy the heart was cut into five to seven slices. The location and size of the infarct was quantitated by computer-assisted planimetry of the slices. The electrocardiogram of 19 (90 percent) of the patients exhibited either a Q wave or an R wave of no more than 20 ms in lead V2. The infarct in the two patients without this electrocardiographic finding was small, occupying 2 and 3 percent of the left ventricle, respectively. The percent infarction of the left ventricle correlated with the QRS point score (r=0.80). Thus in patients without complicating factors in the electrocardiogram and with a single infarct, the electrocardiogram provides a marker for infarction in the anterior third of the left ventricle and permits estimation of infarct size.

In vivo validation of compensatory enlargement of atherosclerotic coronary arteries

Necropsy examinations and epicardial ultrasound studies have suggested that atherosclerotic coronary arteries undergo compensatory enlargement. This increase in vessel size may be an important mechanism for maintaining myocardial blood flow. It also is of fundamental importance in the angiographic study of coronary disease progression and regression. The purpose of this study was to determine, using intracoronary ultrasound, whether coronary arteries undergo adaptive expansion in vivo. Forty-four consecutive patients were studied (30 men, 14 women; mean age 56 +/- 10 years). Eighty intravascular ultrasound images were analyzed (32 left main, 23 left anterior descending and 25 right coronary arteries). Internal elastic lamina area, a measure of overall vessel size increased as plaque area expanded (r = 0.57, p = 0.0001, SEE = 5.5 mm2). When the left main, left anterior descending and right coronary arteries were examined individually, there continued to be as great or greater positive correlation between internal elastic lamina and plaque area (left anterior descending: r = 0.75, p = 0.0001; right coronary arteries: r = 0.63, p = 0.0007; left main: r = 0.56, p = 0.0009), implying that each of the vessels and all in aggregate underwent adaptive enlargement. When only those vessels with < 30% area stenosis were examined, internal elastic lamina correlated well with plaque area (r = 0.79, and p = 0.0001), and for each 1 mm2 increase in plaque area, internal elastic lamina increased 2.7 mm2. This suggests that arterial enlargement may overcompensate for early atherosclerotic lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Percutaneous revascularization of chronic coronary occlusions: An overview

Patients with a chronic coronary occlusion often undergo coronary angiography after weeks to months of occlusion. The published reports underestimate the extent of this problem because such patients are often arbitrarily assigned to receive medical therapy or undergo bypass surgery as a result of poor success with percutaneous revascularization and substantial restenosis. Thus, there is controversy about the role of angioplasty in this patient cohort. The goal of this overview was to evaluate the available information about angioplasty in chronic coronary occlusions. The primary indication for attempted recanalization of a chronic coronary occlusion has been symptomatic angina pectoris. Anginal status often improves after successful procedures (70% vs. 31% with a failed procedure); left ventricular function may improve; and subsequent referral for coronary artery bypass graft surgery is uncommon (3% vs. 28% in unsuccessful cases). Successful recanalization is achieved in approximately 65% of attempted procedures. Inability to cross the stenosis with a guide wire is the most common cause of procedural failure. Statistically significant predictors of procedural success include older occlusions (75% < 3 months old vs. 37% > or = 3 months old), absence of any anterograde flow through the occlusion (76% with vs. 58% without), angiographically abrupt-appearing occlusions (50% vs. 77% with tapered occlusions), presence of bridging collateral vessels (23% with vs. 71% without) and lesions > 15 mm. Procedural complications occur at a slightly lower incidence than in angioplasty of high grade subtotal stenoses. Long-term success is limited, and restenosis can be expected in > 50% of the patients. The experience with chronic total occlusions of saphenous vein bypass grafts is small, but there appear to be limited procedural success and significant procedural complications, particularly associated with distal emboli. The role of new pharmacologic agents has yet to be defined and that of new devices has been disappointing so far, but further technologic advances are on the horizon.

Progression of renal artery stenosis in patients undergoing cardiac catheterization

BACKGROUND Renal artery stenosis is potentially correctable by either revascularization surgery or percutaneous methods. However, appropriate use of these techniques has been hampered by a lack of data on the natural history of this disease. This study assesses the prevalence, risk factors for progression, and effect on renal function of angiographically demonstrated renal artery disease in patients undergoing cardiac catheterization. METHODS The severity of renal artery stenosis was quantified in all patients who underwent abdominal aortography as part of a diagnostic cardiac catheterization study at Duke University Medical Center between January 1989 and February 1996. RESULTS There were 14,152 patients in the study (mean age 61+/-12 years, 62% male). Normal renal arteries were identified in 12,543 (88.7%) patients, insignificant disease (<50% stenosis) in 1 or more vessels in 726 patients (5.1 %), and significant stenosis in 883 patients (6.3%). Significant bilateral renal artery stenosis was present in 178 patients (1.3%). By multivariate logistic regression, elevated serum creatinine level, coronary artery disease, peripheral vascular disease, hypertension, cerebrovascular disease, older age, female sex, and family history of coronary artery disease were identified as independent predictors of significant renal arterial disease. Disease progression was assessed in 1189 patients. Mean time between cardiac catheterizations was 2.6+/-1.6 years. Significant disease progression occurred in 133 patients (11.1 %). Independent predictors of disease progression were female sex, age, coronary artery disease at baseline, and time between baseline and follow-up. At follow-up, serum creatinine level was significantly higher in patients who demonstrated > or =75% stenosis in 1 or more vessels (mean creatinine level 141+114 micromol/L compared with those with insignificant disease (mean creatinine level 97+/-44 micromol/L (P= .01). CONCLUSIONS Renal artery disease is frequently progressive in patients who undergo cardiac catheterization for investigation of coronary artery disease. Significant stenotic disease may develop over a short period despite evidence of normal renal arteries at prior catheterization.

Prognosis in cardiogenic shock after acute myocardial infarction in the intervencional era

OBJECTIVES The purpose of this study is to describe the outcome in cardiogenic shock treated with aggressive reperfusion therapy and to identify factors predictive of in-hospital and long-term mortality. BACKGROUND Cardiogenic shock is the most common cause of death in patients admitted to the coronary care unit. Although studies have reported lower mortality rates in shock treated with angioplasty, few studies have described a cohort of patients with shock who were not selected because they were most likely to benefit from reperfusion therapy. METHODS A consecutive series of 200 patients admitted with acute myocardial infarction complicated by cardiogenic shock were studied. RESULTS The in-hospital mortality rate was 53%. Variables with significant univariable association with in-hospital death included patency of the infarct-related artery, patient age, lowest cardiac index, highest arteriovenous oxygen difference and left main coronary artery disease. The most important independent predictors of in-hospital death were patency of the infarct-related artery, cardiac index and peak creatine kinase, MB fraction. The mortality rate in patients with patent infarct-related arteries was 33% versus 75% in those with closed arteries and 84% in those in whom arterial patency was unknown. Patients who survived to hospital discharge were followed up for a median of 2 years, with a mortality rate of 18% after 1 year. The best descriptors of the relation between these variables and postdischarge mortality included age, peak creatine kinase, ejection fraction and patency of the infarct-related artery. CONCLUSIONS In a large consecutive series of patients with cardiogenic shock with complete follow-up, patency of the infarct-related artery was most strongly associated with in-hospital and long-term mortality. This finding supports an aggressive interventional strategy in patients with cardiogenic shock.

Relation Between Activated Clotting Time During Angioplasty and Abrupt Closure

BACKGROUND The purpose of this study was to determine whether the degree of heparin anticoagulation during coronary angioplasty, as measured by the activated clotting time, is related to the risk of abrupt vessel closure. METHODS AND RESULTS Sixty-two cases of in- and out-of-laboratory abrupt closure in patients in whom intraprocedure activated clotting times were measured were identified from a population of 1290 consecutive patients who underwent non-emergency coronary angioplasty. This group was compared with a matched control population of 124 patients who did not experience abrupt closure. Relative to the control population, patients who experienced abrupt closure had significantly lower initial (median, 350 seconds [25th to 75th percentile, 309 to 401 seconds] versus 380 seconds [335 to 423 seconds], P = .004) and minimum (345 seconds [287 to 387 seconds] versus 370 seconds [321 to 417 seconds], P = .014) activated clotting times. Higher activated clotting times were not associated with an increased likelihood of major bleeding complications. Within this population, a strong inverse linear relation existed between the activated clotting time and the probability of abrupt closure. CONCLUSIONS This study demonstrates a significant inverse relation between the degree of anticoagulation during angioplasty and the risk of abrupt closure. A minimum target activated clotting time could not be identified; rather, the higher the intensity of anticoagulation, the lower the risk of abrupt closure.

Mitral valve replacement for isolated mitral regurgitation: analysis of clinical course and late postoperative left ventricular ejection fraction.

One hundred five patients underwent mitral valve replacement for relief of isolated mitral regurgitation between 1974 and 1979. There were 4 in-hospital deaths (4 percent) and 12 late deaths giving an 82 percent predicted 5 year survival rate. An age of 60 years or more at the time of surgery and a preoperative left ventricular ejection fraction of less than 0.40 were the only variables that correlated with decreased survival at 3 to 5 years after operation (p less than 0.05). Postoperatively, 87 (98 percent) of 89 long-term survivors were in New York Heart Association functional class I or II (68 in class I and 19 in class II). Survival did not differ between patients with porcine versus mechanical valve replacement, but patients with a mechanical valve had a greater incidence of postoperative cerebrovascular accident (8.6/100 patient years) than did patients with a porcine valve (2.8/100 patient years) (p less than 0.002). Ejection fraction at rest was determined with multigated cardiac imaging 12 to 75 months postoperatively in 34 of 89 long-term survivors. The mean preoperative ejection fraction was 0.62 +/- 0.09 (mean +/- 1 standard deviation) and the mean postoperative ejection fraction was 0.50 +/- 0.15 (p less than 0.001). When the preoperative value was compared with the postoperative value at rest the ejection fraction increased by 0.10 or more in 1 patient (3 percent), remained within +/- 0.09 of the preoperative value in 12 patients (35 percent) and decreased by 0.10 or greater in 21 patients (62 percent). Sixteen (94 percent) of 17 patients whose postoperative ejection fraction was greater than 0.50 were in functional class I postoperatively compared with 11 (65 percent) of 17 patients whose postoperative ejection fraction was 0.50 or less (p less than 0.05). No preoperative factor, including preoperative ejection fraction or cardiothoracic ratio, predicted the postoperative ejection fraction. A postoperative exercise ejection fraction was obtained in 29 patients, and an abnormal ejection fraction change with exercise (increase less than 0.05) was observed in 20 patients (69 percent). Patient age at the time of study correlated inversely with the change in ejection fraction from rest to exercise; no other variables were predictive. It is concluded that, in addition to age, only preoperative left ventricular function as measured by ejection fraction predicts survival in patients undergoing mitral valve replacement for isolated mitral regurgitation. Clinical recovery is good even though the majority of long-term survivors have a postoperative decrease in ejection fraction.

Early changes in left ventricular size and function after correction of left ventricular volume overload

The ability to predict early postoperative left ventricular size and function in patients with isolated aortic or mitral regurgitation was determined utilizing multigated blood pool imaging before and 2 to 4 weeks after valve replacement (aortic valve, 20 patients; mitral valve, 20 patients). Early postoperatively, ejection fraction decreased significantly (p <0.001) in both patient groups (from 0.55 ± 12 to 0.40 ± 0.14 [mean ± 1 standard deviation] in patients with aortic regurgitation and from 0.66 ± 0.09 to 0.48 ± 0.11 in patients with mitral regurgitation). The decrease in ejection fraction was associated with a large decrease in stroke volume with minimal or no change in end-systolic volume; it was unrelated to the preoperative ejection fraction. Early postoperative ejection fraction correlated best with preoperative end-systolic volume and was normal in 14 (67 percent) of 21 patients with a preoperative ejection fraction above 0.60; 4 (27 percent) of 15 patients with a preoperative ejection fraction of 0.50 to 0.60; and in 0 of 4 patients with a preoperative ejection fraction below 0.50 (p <0.05). In addition, a repeated scan in 16 patients late (1 to 2 years) after operation showed a further reduction in endsystolic volume in patients with aortic regurgitation with an increase in ejection fraction toward preoperative values. There was no significant change in patients with mitral regurgitation. End-diastolic volume decreased significantly (p <0.001) early postoperatively (from 162 ± 60 to 102 ± 41 ml/m2 in patients with aortic regurgitation and from 131 ± 40 to 78 ± 30 ml/m2 in patients with mitral regurgitation). This decrease was closely related to a decrease in stroke volume and was unrelated to preoperative ejection fraction. Early postoperative end-diastolic volume correlated best with the preoperative end-systolic volume. The major part of the reduction in end-diastolic volume occurred within 2 weeks of valve replacement. Removal of chronic left ventricular volume overload due to aortic or mitral regurgitation produces a decrease in ejection fraction and end-diastolic volume. The early reduction is in part a result of altered loading conditions and may not necessarily imply alterations in myocardial contractile function. The reduction in ejection fraction appears to persist in patients with mitral regurgitation.