Iron deficiency anemia and cardiac mortality in patients with left ventricular systolic dysfunction undergoing coronary stenting.

AIM: The aim of this study was to assess cardiac mortality in patients with reduced ejection fraction (EF< or =45%) and anemia (Hb< or =12 g/dL) undergoing coronary stenting and to investigate whether iron-deficiency anemia influenced outcome when compared to non-anemic patients or patients with other types of anemia. METHODS: One hundred twenty consecutive patients undergoing percutaneous coronary intervention (PCI) between April 2003 and December 2005 were identified and followed for a median of 30 months. Patients were divided into 2 groups, anemic (Hb< or =12 g/dL) and non-anemic. Anemic patients were then divided into 3 sub-groups based on laboratory analysis and anemia work-up: iron-deficiency, malignancy-associated, and anemia of chronic disease (including chronic kidney disease). Mortality rates and cause of death were retrieved using both the Social Security database and the hospital records. RESULTS: Thirty-one percent of patients had iron deficiency, 24% had a malignancy-associated anemia and 45% had anemia of chronic disease. Overall mortality was 12% of which 29% was cardiac death. All-cause and cardiac mortality were significantly higher in anemic vs. non-anemic patients, (31% vs. 6%, P<0.001, and 10% vs. 1%, P=0.016, respectively). Iron-deficiency anemia strongly predicted cardiac mortality (33% vs. 1% in non-anemic patients, P<0.001), while malignancy-associated anemia was the strongest predictor of non-cardiac death (57% vs. 4% in non-anemic patients, P<0.001). Anemia of chronic disease neither predicted cardiac nor non-cardiac death. CONCLUSIONS: To the authors' knowledge, this is the first study to show that iron-deficiency anemia is a strong predictor of cardiac death when compared to patients with other types of anemia or to non-anemic patients.

Angiographic morphology of coronary artery stenoses in prolonged rest angina: evidence of intracoronary thrombosis.

Previous clinical and angiographic/histopathologic correlative studies have demonstrated that angiographic findings of occlusive thrombus, intraluminal filling defects and complex lesion morphology indicate the presence of intracoronary thrombosis. The purpose of this study was to determine whether the presence of these descriptors of intracoronary thrombosis is associated with the syndrome of prolonged rest angina. The coronary angiograms of 50 patients with prolonged rest angina without myocardial infarction (group I) and 42 concurrent patients with stable angina (group II) were reviewed without knowledge of the clinical syndrome. Patients with prior myocardial infarction, coronary angioplasty or coronary artery bypass graft surgery were excluded, as were patients with important aortic stenosis. Each coronary artery stenosis in a major epicardial vessel was evaluated for the presence or absence of intracoronary thrombus (defined using standard criteria), complex lesion morphology (defined as the presence of haziness, a smudged appearance or irregular lesion margins) and eccentricity, and the frequency of each of these findings in groups I and II was compared. Intracoronary thrombus was present significantly more often in group I patients (42%) than in group II patients (17%) (chi 2 5.77; p less than 0.02). Complex lesion morphology was also present significantly more often in group I (44%) than in group II (14%) patients (chi 2 8.17; p less than 0.01). Either standard criterion for intracoronary thrombus or complex morphology was present in 70% of group I but only 21% of group II patients (chi 2 19.7; p less than 0.001). These results support a strong association of the angiographic descriptors of intraluminal thrombosis with the clinical syndrome of prolonged rest angina.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute changes in global and regional rest left ventricular function after successful coronary angioplasty: comparative results in stable and unstable angina.

The immediate effects of successful percutaneous transluminal coronary angioplasty on global and regional left ventricular function were assessed by comparing 30 degrees right anterior oblique left ventricular angiograms performed immediately before and after angioplasty on 39 patients undergoing 42 successful procedures. Mean (+/- SD) lesion stenosis decreased from 88 +/- 10% to 35 +/- 11% (p less than or equal to 0.001), whereas left ventricular ejection fraction increased from 57 +/- 11% to 64 +/- 10% (p less than or equal to 0.001) for the entire group. Left ventricular functional changes were further subgrouped according to stability of angina. Eighteen procedures were performed on 17 patients with stable angina: 24 procedures were performed on 22 patients with unstable angina defined as angina at rest or on minimal activity or recently accelerated angina. There were no significant subgroup differences in mean age, gender ratio, vessel anatomy, drug therapy or extent of coronary stenosis before or after angioplasty. Global ejection fraction increased significantly for the unstable group (from 54 +/- 11% to 66 +/- 9%, p less than or equal to 0.001) but was unchanged for the stable group (from 61 +/- 9% to 61 +/- 11%, p = NS). In unstable angina, regional ejection fraction (segmental area method) increased for both jeopardized (from 37 +/- 11% to 52 +/- 9%, p less than or equal to 0.001) and nonjeopardized myocardial segments (from 43 +/- 13% to 51 +/- 13%, p less than or equal to 0.001), but improvement was significantly (p less than or equal to 0.02) greater in jeopardized segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary angioplasty in patients with severe left ventricular dysfunction.

The applications for coronary angioplasty have greatly expanded and the procedure is now increasingly used in complex and potentially high risk conditions. This report describes the short- and long-term effects of coronary angioplasty in 61 patients with severely depressed left ventricular function (ejection fraction less than or equal to 35%) with unstable or refractory anginal symptoms, or both, in whom revascularization was necessary despite increased risk. In a retrospective analysis of 1,260 patients undergoing angioplasty between January 1985 through December 1987, 61 had an ejection fraction less than or equal to 35%. The common clinical presentation was unstable angina (70%) with or without recent myocardial infarction. Mean left ventricular ejection fraction was 27 +/- 6%. Forty-five patients (74%) had multivessel disease. Clinical success after angioplasty was achieved in 55 patients (90%). Major complications (death, infarction and emergency bypass surgery) occurred in five patients (8.2%), with death in two (3.2%). During long-term (mean 21 +/- 11 months) follow-up study of the 55 patients with successful angioplasty, 13 (23%) died, including 3 of noncardiac causes, and 11 (20%) had clinically symptomatic recurrence. Continued clinical success was present in 39 patients (71%), of whom 28 (51%) were event-free patients and 11 (20%) had clinical recurrence; a successful second angioplasty procedure was performed in 9 because of restenosis. Thus, in patients with depressed left ventricular function, coronary angioplasty can be performed with a short-term success rate comparable to that of routine angioplasty or surgical procedures. However, acute complications are more frequent and the late mortality rate is higher than in patients with less depressed function.

Triple vessel coronary angioplasty: acute outcome and long-term results.

Triple vessel coronary angioplasty, defined as angioplasty of one or more lesions in each of the three major coronary arteries (left anterior descending, left circumflex, right coronary artery) was performed in 50 (11%) of 469 patients who had angioplasty of multiple vessels. There were 32 men and 18 women with a mean age of 56 years. All 50 patients had severe three vessel coronary disease and represent approximately 5% of patients with three vessel disease who had revascularization in this institution; 8 (16%) had previous coronary bypass surgery, and 23 (46%) had previous myocardial infarction. Unstable angina was present in 33 patients (66%) and 96% had Canadian Heart Association class III or IV angina; mean left ventricular ejection fraction was 57 +/- 11%. Angioplasty was performed in 176 vessels (3.5 vessels per patient, range 3 to 6) and in 250 lesions (5 lesions per patient, range 3 to 9); angiographic success was achieved in 240 lesions (96%) and 166 vessels (94%). Success in all vessels attempted was achieved in 40 (80%) of the 50 patients. Clinical success (angiographic success associated with clinical improvement) was obtained in all 50 patients in whom triple vessel angioplasty was performed; none of them required urgent bypass surgery and 5 patients (10%) had a non-Q wave myocardial infarction. In four other patients triple vessel angioplasty was planned but not performed because of failure to dilate the primary vessel; urgent bypass surgery was required in one of these, who developed a Q wave infarction. Thus, overall clinical success in 54 patients was 93%; the incidence rate of myocardial infarction was 11%, and that of urgent surgery 1.8%.(ABSTRACT TRUNCATED AT 250 WORDS)

Multivessel coronary angioplasty early after acute myocardial infarction.

Coronary angioplasty has been applied in patients with recent myocardial infarction, but results of angioplasty of multiple vessels early after myocardial infarction in patients with severe multivessel disease have not been reported. Coronary angioplasty of multiple vessels was performed in 105 patients 0 to 15 days (mean 5 +/- 4) after recent myocardial infarction. There were 77 men (73%) and 28 women (27%), with a mean age of 57 years. All patients had severe multivessel disease, 68% with two vessel and 32% with three vessel disease. Twenty-eight patients (27%) had successful thrombolysis before angioplasty and 70 (67%) had postinfarction angina. Mean left ventricular ejection fraction was 58 +/- 10% and was less than 45% in 13 patients (12%). Angioplasty was attempted in 319 lesions (mean 3 lesions per patient, range 2 to 9) and 252 vessels (mean 2.4 vessels per patient, range 2 to 4), with success in 302 lesions (95%) and 237 vessels (94%); angioplasty was done in two stages in 59 patients (56%). Clinical success was achieved in 102 patients (97%). Complications included myocardial infarction in six patients (5.7%) (one Q wave, five non-Q wave), urgent bypass surgery in two (1.9%) and death in one (0.9%); overall, seven patients (7%) had a major complication. All patients had a follow-up duration greater than 1 year (mean 31 months, range 12 to 73). Clinical recurrence developed in 24 patients (23%), of whom 21 had repeat angioplasty, 1 had bypass surgery and 2 were managed medically. Ten patients (9.8%) had a late infarction and 5 (4.9%) died of cardiac death during the follow-up period.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical and angiographic determinants of primary coronary angioplasty success. M-HEART Investigators.

Clinical and anatomic determinants of the initial success of percutaneous transluminal coronary angioplasty were prospectively evaluated in 826 patients enrolled in the Multi-Hospital Eastern Atlantic Restenosis Trial (M-HEART). The 639 men and 187 women ranged in age from 31 to 85 years. Successful angioplasty (residual stenosis less than 50% and no major complications) was achieved in 886 (88.6%) of 1,000 lesions. Success rates were uniform among the eight individual centers. Outcome was not influenced by gender, age or other clinical features, including severity and duration of angina, prior myocardial infarction, rest pain, transient ST segment elevation, history of smoking or diabetes. In contrast, procedural outcome was significantly associated with lesion-specific angiographic factors. Stenoses 60% to 74%, 75% to 89%, 90% to 99% and 100% were associated with success rates of 96%, 90%, 84% and 69%, respectively (p less than 0.001). Angioplasty was less successful in calcified than in noncalcified lesions (82% versus 90%, p less than 0.01), in thrombotic than in nonthrombotic lesions (82% versus 90%, p less than 0.05) and in lesions in the right coronary artery than in other vessels (84% versus 90%, p less than 0.01). Outcome was not related to other anatomic variables, including lesion location (proximal versus distal), vessel size, eccentricity, stenosis length or translesional gradient. By multivariate logistic regression, preangioplasty percent stenosis, right coronary artery location and lesion calcification were demonstrated to be significant independent predictors of angioplasty success. Alternative clinical and angiographic variables did not contribute to this regression model.(ABSTRACT TRUNCATED AT 250 WORDS)

Restenosis after coronary angioplasty: a multivariate statistical model to relate lesion and procedure variables to restenosis. The M-HEART Investigators.

The Multi-Hospital Eastern Atlantic Restenosis Trial group obtained follow-up angiography in 510 patients with 598 successfully dilated coronary lesions who were enrolled in a controlled trial of the effects of a single dose of 1 g of methylprednisolone on restenosis after coronary angioplasty. The overall restenosis rate was 39.6%. The strongest univariate relations to the restenosis rate were found for lesion location (saphenous vein graft, 68%; left anterior descending artery, 45%; left circumflex artery and right coronary artery, 32%; p = 0.002); lesion length (less than or equal to 4.6 mm, 33%; greater than 4.6 mm, 45%; p = 0.001); percent stenosis before angioplasty (less than or equal to 73%, 25%; greater than 73%, 43%; p = 0.005), percent stenosis after angioplasty (less than or equal to 21%, 33%; greater than 21%, 46%; p = 0.017) and arterial diameter (less than 2.9 mm, 44%; greater than or equal to 2.9 mm, 34%; p = 0.036). Two multivariate models to predict restenosis probability were developed with use of stepwise logistic regression. The preprocedural model, which included only variables whose values were known before angioplasty, entered lesion length, vein graft location, left anterior descending artery location, percent stenosis before angioplasty, eccentric lesion and arterial diameter. The postprocedural model, which also included variables whose values were known after angioplasty was performed, was similar to the preangioplasty model except that it also entered postangioplasty percent stenosis and "optimal" balloon sizing but did not enter eccentric lesion. These data indicate that the probability of restenosis after angioplasty is determined predominantly by the characteristics of the lesion being dilated. They are consistent with the known intimal proliferative mechanism of restenosis, offer a means of identifying lesions at unusually high or low risk of restenosis, and of predicting the likelihood that a particular lesion will restenose after angioplasty and provide a rationale for stratification by restenosis probability in the design of future studies of restenosis.

Adverse reactions of low osmolality contrast media during cardiac angiography: a prospective randomized multicenter study.

A multicenter study was performed to determine the incidence of adverse reactions to two contrast media with similar low osmolality during cardiac angiography. The study was of a randomized double-blind design comparing ioxaglate (an ionic dimer) and iopamidol (a nonionic compound) and included 500 patients; 250 patients received ioxaglate and 250 iopamidol. There were 58 adverse reactions attributed to the contrast media in the ioxaglate group and 29 in the iopamidol group (p less than 0.001). Chest pain occurred in 11 patients in the ioxaglate group compared with 5 in the iopamidol group (p = 0.123). Nausea or vomiting was present in 20 and 2 patients, respectively (p less than 0.0003). Allergic adverse reactions, such as bronchospasm, urticaria and itching, occurred in 15 of the ioxaglate group and only 1 of the patients receiving iopamidol (p less than 0.0007). Fifty-two patients in the ioxaglate group had a known allergic history (not to contrast medium) or asthma, whereas 77 receiving iopamidol had a similar history. Seven of the 52 ioxaglate-treated patients developed an allergic adverse reaction compared with none of the 77 in the iopamidol group (p = 0.001). Of 41 patients receiving ioxaglate who were premedicated with diphenhydramine, 4 had an allergic adverse event. In the iopamidol group 45 patients received similar premedication and none had an allergic adverse reaction (p less than 0.03). Thus, this multicenter study shows that adverse reactions occur more often with ioxaglate than with iopamidol and that patients with an allergic history have a greater risk with ioxaglate therapy compared with iopamidol.

Myocardial contrast echocardiography for the assessment of coronary blood flow reserve: validation in humans.

OBJECTIVES: The aim of this study was to validate the use of myocardial contrast echocardiography to determine coronary blood flow reserve in humans. BACKGROUND: Although myocardial contrast echocardiography has been used to accurately quantify coronary flow reserve in animals, validation for its use in humans to measure flow reserve is lacking. METHODS: We analyzed the time-intensity curve from the anteroseptal region of the left ventricular short axis produced after a left main coronary artery injection of sonicated albumin before and after intracoronary administration of papaverine in 16 patients without angiographically significant coronary artery disease. The ratio of half-time of video intensity disappearance from peak intensity, variable of curve width, area under the time-intensity curve and corrected peak contrast intensity after papaverine compared with baseline were correlated with coronary flow reserve measured simultaneously with an intracoronary Doppler probe in the left anterior descending coronary artery. RESULTS: There was a strong inverse correlation with half-time of contrast washout and coronary flow reserve (r = -0.76, p = 0.0007) and a strong positive correlation between the variable of curve width (which is inversely proportional to curve width) and coronary flow reserve (r = 0.71, p = 0.002). There was a weak but significant inverse correlation between area under the time-intensity curve and coronary flow reserve (r = -0.54, p = 0.03) but no correlation between corrected peak contrast intensity and coronary flow reserve (r = -0.36, p = NS). Despite the strong correlation for the ratios for half-time of contrast washout and variable of curve width and actual coronary flow reserve measured with intracoronary Doppler probe, the transit time ratios consistently underestimated coronary flow reserve. CONCLUSIONS: Myocardial contrast echocardiography performed with left main coronary artery injections of sonicated albumin can be utilized to measure coronary flow reserve in humans. Transit time variable ratios (half-time of contrast washout and variable of curve width) derived from the time-intensity curve correlate most strongly with coronary flow reserve.

Impedance cardiograms reliably estimate beat-by-beat changes of left ventricular stroke volume in humans.

Linear regression was used to compare stroke volumes calculated from tetrapolar impedance cardiograms and simultaneous left ventriculograms in 14 patients undergoing diagnostic left heart catheterisation. We calculated three to five consecutive stroke volumes from each ventriculogram. Left ventricular stroke volumes estimated by the two methods correlated closely: the correlation coefficients from pairs of data obtained from individual patients ranged between 0.77 and 1.00 (average = 0.91), and the correlation coefficient for pooled data (all pairs from all subjects) was 0.79 (p less than 0.001). Changes in left ventricular stroke volume measured with the two methods also correlated well (r = 0.89 for pooled data, p less than 0.001). The results suggest that impedance cardiograms provide reliable estimates of changes of beat-by-beat left ventricular stroke volumes and reasonable estimates of absolute levels of beat-by-beat stroke volumes in humans.

Once-daily therapy for angina pectoris with nifedipine gastrointestinal therapeutic system. Dosing and clinical efficacy.

The nifedipine gastrointestinal therapeutic system (GITS) is a promising new formulation that provides continuous release of nifedipine over the course of 24 hours with once-daily dosing. Results from a 14-week, open-label, crossover multicenter trial completed by 91 patients with chronic stable angina pectoris demonstrate that patients treated with standard nifedipine capsules may be switched to equivalent total 24-hour doses of nifedipine GITS and achieve comparable or improved efficacy (due to improved compliance) with a more favorable side-effects profile. Furthermore, in a subset of 10 patients who underwent sequential exercise testing, exercise responses obtained throughout 12 weeks of treatment with nifedipine GITS were comparable to measurements obtained during treatment with nifedipine capsules and demonstrated that tolerance did not occur. These patients also experienced significantly fewer vasodilatory side effects during treatment with nifedipine GITS compared with nifedipine capsules. Thus, nifedipine GITS represents a sound pharmacologic approach to the management of ischemic disease; and with once-daily dosing and a favorable side-effect profile this agent affords the potential for better patient compliance and efficacy without concern about the development of tolerance.

Alternative medical treatment for patients with angina pectoris and adverse reactions to beta blockers. Usefulness of nifedipine.

Although beta blockers are effective for the treatment of angina pectoris, chronic adverse effects produced by these agents--including lethargy, fatigue, and male impotence--can adversely affect patient acceptance and treatment compliance. To assess the clinical effects of switching from anti-anginal treatment with beta blocker only (phase I) to half-dose beta blocker plus the calcium blocker nifedipine (phase II) or nifedipine alone (phase III), 18 patients with chronic stable angina pectoris and side effects to beta blockers were evaluated in a 12-week, open-label trial. Three patients did not complete the study, one secondary to new unstable angina and two secondary to nifedipine side effects. Of the 15 patients completing the trial (13 men and two women; mean age, 54 +/- 5 [SEM] years), all sequentially participated in the one-month phases. Weekly angina frequency assessed from patient diaries was significantly less for treatment with nifedipine only (phase III) as compared with beta blocker (phase I) (1.7 +/- 1 versus 3.9 +/- 1 episodes per week), while phase II was not significantly different. Exercise test time was maintained throughout all phases (phase I, 457 +/- 39; phase II, 458 +/- 40; and phase III, 498 +/- 48 seconds, p not significant). All 15 patients in phase I (100 percent) had side effects to beta blockers, but these side effects were lessened in 12 patients (80 percent) in phase II and 13 patients (86 percent) in phase III, with total alleviation of symptoms in two patients (13 percent) in phase II, and eight patients (53 percent) in phase III. Thus, in patients with side effects to beta blockers, switching to nifedipine is associated with a significant reduction in beta blocker adverse symptoms and equal anti-anginal efficacy.

Nifedipine gastrointestinal therapeutic system in stable angina pectoris. Results of a multicenter open-label crossover comparison with standard nifedipine.

To compare the clinical efficacy and dose equivalency of standard nifedipine versus a new gastrointestinal therapeutic system (GITS) formulation of nifedipine, 98 patients with chronic stable angina pectoris participated in a 14-week, multicenter, open-label, crossover trial. All patients were administered nifedipine capsules for one month prior to study entry and continued receiving other antianginal, non-calcium blocker medications. Ninety-one patients (93 percent), 80 men and 11 women, mean age 62 +/- 1 years, completed the trial, which included two weeks receiving standard nifedipine followed by 12 weeks receiving nifedipine GITS starting at a dosage equal to the 24-hour total dose of nifedipine capsules and titrated upward as necessary. However, throughout the trial, mean nifedipine dosage was similar on nifedipine GITS compared with standard nifedipine. Angina frequency was significantly less with nifedipine GITS at Weeks 6, 10, and 14 (0.8 episodes/week) compared with baseline with standard nifedipine (1.3 episodes/week, p less than 0.05). Likewise, nitroglycerin consumption was also less at Weeks 6, 10, and 14, but only significantly less at Week 6 (nifedipine 1.2/week versus nifedipine GITS at six weeks, 0.7/week; p less than 0.05). Resting hemodynamic parameters, including systolic and diastolic blood pressure and heart rate, were not significantly different with standard nifedipine versus nifedipine GITS during the 12-week study. Total incidences of side effects were similar for both treatments (standard nifedipine, 16; nifedipine GITS, 17). However, incidence of vasodilator side effects (flushing, dizziness, and light-headedness) was significantly less frequent with nifedipine GITS (standard nifedipine, 12; nifedipine GITS, six; p less than 0.05). Thus, results from this open-label, crossover trial suggest that nifedipine GITS dosing is similar to multidose standard nifedipine with equivalent 24-hour efficacy for nifedipine GITS.

Evolving applications of coronary angioplasty: technical and angiographic considerations.

Coronary angioplasty (PTCA) is now applicable to selected patients with multiple vessel disease, total occlusions, tandem lesions and complex branch disease. Operator experience and skill contribute to a high success rate in complex anatomy, but equally important is appropriate case selection based on angiographic review of lesion morphology, branches, extent of coronary artery disease, and left ventricular function. Likewise, during and after the procedure similar angiographic assessment is important to determine resultant lesion morphology, branch anatomy, distal runoff, and adequacy of lesion dilatation. Thus, the outcome of angioplasty is dependent on the operator's ability to opacify the coronary arteries with minimal or no vessel/lesion overlap or foreshortening. Although coronary angiography has become more routine for many angiographers with the advent of angioplasty, the importance of high-quality angiography continues to be a major component for successful angioplasty.

Hemodynamic and electrophysiologic effects of first- and second-generation calcium antagonists.

The calcium antagonists currently available exert significantly different in vitro and in vivo electrophysiologic, hemodynamic, and contractile effects on cardiovascular function, mediated through differential cardiac and vascular smooth muscle responses to calcium channel blockade. These differences have important implications regarding choice of agent in specific clinical conditions, such as sinus or atrioventricular nodal disease, depressed left ventricular function, or congestive heart failure--conditions that may coexist with angina or hypertension. Recognizing and utilizing the properties of the different calcium antagonists is important to ensure maximally effective clinical outcomes. For example, in patients with hypertrophic cardiomyopathy and supraventricular arrhythmias, verapamil is singularly effective, whereas in post-myocardial infarction patients with pulmonary congestion, diltiazem may produce an added risk. Calcium antagonists of the dihydropyridine class, such as nifedipine and amlodipine, have the greatest peripheral vasoselective effects and thus the greatest potential to reduce afterload, minimizing direct left ventricular depression of contractility. Despite favorable effects of calcium antagonists, most of the agents currently available are not clearly safe in congestive heart failure and may adversely affect left ventricular function. However, newer calcium antagonists such as amlodipine are being investigated with regard to their safety in congestive heart failure.

Changing concepts in the pathophysiology of myocardial ischemia.

The principal common pathway for myocardial ischemia is an oxygen supply-demand imbalance; more recently, greater emphasis has been placed on limitations of myocardial blood supply, as well as excessive myocardial oxygen demand. Myocardial ischemia is a metabolic event resulting from inadequate oxygen delivery to local tissues. The physiologic effects of ischemia are observed through abnormalities in left ventricular function, electrocardiographic changes, and often, by angina pectoris. Prognostic and therapeutic outcomes are significantly related to the pathophysiology of the underlying coronary lesion. Because myocardial ischemia often occurs without symptoms, clinical distinctions based on angina stability may more appropriately be represented by stable or unstable ischemic syndromes that incorporate silent ischemia. Stable ischemic syndromes occur secondary to coronary plaques, whereas unstable syndromes are the result of active lesions caused by plaque rupture with local thrombus and vasoreactivity that produce intermittent critical decreases in coronary supply. The prognosis of patients with stable ischemia is related to the extent of myocardium at jeopardy and overall left ventricular function. In contrast, unstable syndromes are associated with a worse short-term prognosis, which may be predictable by the presence of silent ischemia or left ventricular dysfunction or both. Therapeutic decisions based on an improved pathophysiologic understanding of ischemic mechanisms as well as the physiologic impact of therapy on cardiac function can enhance efficacy while avoiding adverse effects. Calcium channel blockers appear to afford certain advantages in the treatment of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute electrophysiologic, hemodynamic and left ventricular effects of nifedipine and beta-blocker interactions. Maintenance of global and regional left ventricular wall motion.

To assess potential cardiac effects of nifedipine and beta-blocker interactions, 10 men receiving chronic beta-blocker therapy for angina underwent hemodynamic, electrophysiologic and left ventricular (LV) functional analyses at the time of cardiac catheterization before and after buccal administration of 10 mg of nifedipine. Although this combination is usually well tolerated, there have been occasional reports suggesting that the combination of nifedipine and beta-blocking agents may increase the likelihood of congestive heart failure, severe hypotension or exacerbation of angina. All patients had class II or III stable angina pectoris and were receiving at least 160 to 240 mg/day of propranolol or equivalent doses of beta-blocker therapy. Nifedipine produced no acute electrophysiologic changes, including heart rate, PR interval, AH interval, HV interval, sinus node recovery time or heart rate at which atrioventricular nodal block occurred. Hemodynamic effects included no significant change in mean right atrial pressure (7 +/- 1 vs 5 +/- 1 mm Hg), while mean pulmonary artery pressure decreased significantly (20 +/- 2 vs 17 +/- 1 mm Hg, p less than or equal to 0.05). In addition, LV end-diastolic pressure decreased significantly from 16 +/- 2 to 10 +/- 1 mm Hg (p less than or equal to 0.05), with a nonsignificant decrease in mean aortic pressure from 93 +/- 5 to 86 +/- 4 mm Hg. Likewise, no significant change occurred in cardiac index (3.2 +/- 0.4 vs 3.0 +/- 0.4 liters/min/m2) or systemic vascular resistance (1,157 +/- 247 vs 1,170 +/- 236 dynes/s/cm-5). Left ventricular ejection fraction (EF) was the same before and after nifedipine (73 +/- 2% vs 74 +/- 2%).(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of angiographic findings and demographic variables in patients with coronary artery disease presenting with acute pulmonary edema versus those presenting with chest pain.

One hundred nineteen patients admitted to the coronary care unit with pulmonary edema were retrospectively reviewed to identify the demographic characteristics and underlying cardiac disorders of this population. The patients with pulmonary edema were compared with 119 patients admitted to the coronary care unit with chest pain. Cardiac catheterization in 71 patients with pulmonary edema and 93 with chest pain showed left main and 3-vessel coronary artery diseases to be equally common in both groups, although anginal pain was infrequent in patients with pulmonary edema (n = 28, 24%). Left ventricular function was reduced in the patients with pulmonary edema compared with those with chest pain (mean ejection fraction 42 vs 59%; p less than 0.001). More patients with pulmonary edema were black, and had diabetes and preexisting hypertension than those with chest pain. The results of cardiac catheterization were the same for black and white patients with pulmonary edema. In conclusion, patients with pulmonary edema have a high incidence of cardiac disease, and pulmonary edema may be 1 manifestation of silent myocardial ischemia. Important demographic differences exist between patients admitted with pulmonary edema and those who present with chest pain.

Angiographic patterns of restenosis after angioplasty of multiple coronary arteries.

To assess angiographic patterns of restenosis after percutaneous transluminal coronary angioplasty (PTCA) of multiple coronary arteries, angiograms were reviewed in 40 patients with clinical recurrence after PTCA of multiple arteries. Clinical recurrence was defined as return of symptoms after successful PTCA of more than 1 major artery or branch and angiographic evidence of restenosis of 1 or more lesions. In these 40 patients, 83 arteries (2.1 arteries per patient) and 103 narrowings (2.6 narrowings per patient) were successfully dilated. Restenosis developed in 57 of 83 arteries at risk (69%): 23 patients (58%) had restenosis in only 1 artery and 17 (42%) in 2 arteries. Restenosis occurred in 63 of 103 lesions at risk (61%): 20 patients (50%) had restenosis of 1 narrowing, 17 (43%) had restenosis of 2 narrowings and 3 (7%) had recurrence of 3 narrowings. Only 13 patients (33%) had restenosis of all narrowings dilated. Predictors of restenosis of individual narrowings were: higher pre-PTCA percent stenosis (87 +/- 10% in narrowings with restenosis vs 82 +/- 10% in narrowings without, p less than 0.02), and higher degree of residual stenosis after PTCA (46 +/- 13% in narrowings with restenosis vs 36 +/- 12% in narrowings without, p less than 0.001). Balloon size or inflation pressure did not predict recurrence of narrowings. Repeat PTCA was successful in 97% of cases attempted (33 of 34), 3 patients underwent elective bypass surgery and 3 were managed with medical therapy. Most patients with clinical recurrence after PTCA of multiple arteries do not have restenosis of multiple arteries or narrowings, and only one-third will have recurrence of all narrowings.(ABSTRACT TRUNCATED AT 250 WORDS)