Intravenous amiodarone for the prevention of atrial fibrillation after open heart surgery: the Amiodarone Reduction in Coronary Heart (ARCH) trial.

OBJECTIVES: This study was designed to test whether intravenous (i.v.) amiodarone would prevent atrial fibrillation and decrease hospital stay after open heart surgery. BACKGROUND: Atrial fibrillation commonly occurs after open heart procedures and is thought to be a significant determinant for prolongation of hospitalization. Oral amiodarone given preoperatively appears to reduce the incidence of atrial fibrillation. This study was designed to test whether the more rapid-acting i.v. formulation of amiodarone given postoperatively would reduce the incidence of atrial fibrillation. METHODS: Three hundred patients undergoing standard open heart surgery were randomized in a double-blind fashion to i.v. amiodarone (1 g/day for 2 days) versus placebo immediately after open heart surgery. The primary end points of the trial were incidence of atrial fibrillation and length of hospital stay. Baseline clinical variables and mortality and morbidity data were collected. RESULTS: Atrial fibrillation occurred in 67/142 (47%) patients on placebo versus 56/158 (35%) on amiodarone (p = 0.01). Length of hospital stay for the placebo group was 8.2 +/- 6.2 days, and 7.6 +/- 5.9 days for the amiodarone group (p = 0.34). No differences were noted in baseline variables, morbidity or mortality. CONCLUSIONS: Low-dose i.v. amiodarone was safe and effective in reducing the incidence of atrial fibrillation after heart surgery, but did not significantly alter length of hospital stay.

Attenuation of the circadian patterns of myocardial ischemia with nifedipine GITS in patients with chronic stable angina. N-CAP Study Group.

The Nifedipine Gastro-Intestinal Therapeutic System (GITS) Circadian Anti-ischemia Program (N-CAP) was designed to test the effect of nifedipine GITS as monotherapy or in combination with a beta-adrenergic blocking agent on the circadian pattern of angina and silent ischemia in patients with chronic stable angina. At 118 sites in the United States, 1,174 patients were screened for entry into this study. To be eligible for participation patients were required to have at least two episodes of angina a week and at least two episodes of myocardial ischemia during 48-h ambulatory electrocardiographic (ECG) monitoring during the baseline placebo period. A total of 207 patients completed all phases of the study. Beta-blockers were continued in those patients already receiving them. In this 7- to 10-week single-blind placebo withdrawal study, a 1-week placebo run-in was followed by up to 5 weeks of single-blind titration with nifedipine GITS, a 4-week efficacy phase with an established dose and a final single-blind 2-week placebo withdrawal period. Ambulatory ECG monitoring was performed at the end of each placebo phase and at the end of the efficacy phase with a digital monitoring device that was validated in a pilot study. Overall, nifedipine GITS significantly reduced the weekly number of anginal episodes from 5.7 to 1.8 (p = 0.0001) and the number of ischemic events from 7.3 to 4 (p = 0.0001) reported during the 48-h monitoring periods, with a significant increase in both during the placebo withdrawal period. The baseline circadian pattern of ischemia showed an early morning peak and a secondary peak in the afternoon. Nifedipine GITS significantly reduced ischemia during the 48-h period when administered as monotherapy or in combination with a beta-blocker. Patients were also randomized to receive nifedipine GITS in either a morning or an evening dose. The two regimens resulted in equal anti-ischemic benefit. The primary side effect of nifedipine GITS was edema, which was dose related. In summary, nifedipine GITS reduced the number of anginal and ischemic episodes when given alone or in combination with a beta-blocker. Nifedipine GITS had a sustained effect: a single daily dose was effective over 24 h regardless of whether it was administered in the morning or evening. This study also suggests that combination therapy with nifedipine GITS and a beta-blocker is especially efficacious in reducing ischemia.

Silent ischemia predicts infarction and death during 2 year follow-up of unstable angina.

Silent myocardial ischemia as detected on Holter electrocardiographic (ECG) monitoring is present in greater than 50% of patients with unstable angina despite intensive medical therapy. The presence and the extent of silent ischemia have been correlated with an increased risk of early (1 month) unfavorable outcome including myocardial infarction and need for coronary revascularization for persistent symptoms. Seventy patients with unstable angina who had undergone continuous ECG monitoring for silent ischemia were followed up for 2 years; 37 patients (Group I) had Holter ECG evidence of silent ischemia at bed rest in the coronary care unit during medical treatment with nitrates, beta-receptor blockers and calcium channel antagonists; the other 33 patients (Group II) had no ischemic ST segment changes (symptomatic or silent) on Holter monitoring. Over a 2 year follow-up period, myocardial infarction occurred in 10 patients in Group I (in 2 it was fatal) compared with one nonfatal infarction in Group II (p less than 0.01 by Kaplan-Meier analysis); revascularization with either coronary bypass surgery or angioplasty for symptomatic ischemia was performed in 11 Group I and 5 Group II patients (p less than 0.05). Multivariate Cox's hazard analysis demonstrated that the presence of silent ischemia was the best predictor of 2 year outcome. Therefore, persistent silent myocardial ischemia despite medical therapy in patients with unstable angina carries adverse prognostic implications that persist over a 2 year period.

Acute nifedipine withdrawal: consequences of preoperative and late cessation of therapy in patients with prior unstable angina.

Reports of acute ischemic events after withdrawal of calcium antagonist therapy in outpatients and during bypass surgery in patients with prior angina at rest prompted the examination of the effect of nifedipine withdrawal in 81 patients who had completed a prospective, double-blind randomized trial of nifedipine versus placebo for rest angina. Thirty-nine patients underwent bypass surgery for uncontrolled angina or left main coronary artery disease. No significant difference between patients withdrawn from nifedipine or placebo was seen in the incidence of perioperative myocardial infarction, hypotension requiring intraaortic balloon counterpulsation, vasopressor or vasodilator requirements or incidence of significant arrhythmias. An additional 42 patients had completed 2 years on a protocol consisting of nitrates and propranolol in addition to nifedipine or placebo. During a mean of 66 hours of continuous monitoring after withdrawal of nifedipine or placebo, heart rate and blood pressure were unchanged. A worsening of previously present angina at rest occurred in five patients who had continued to experience rest angina before drug withdrawal, four of whom were withdrawn from nifedipine. No patient with class I to III angina experienced new onset of rest angina during drug withdrawal. No patient experienced myocardial infarction. There was no significant difference between patients withdrawn from nifedipine or placebo in the duration or frequency of ischemic ST changes on continuous electrocardiographic monitoring, or in duration or positive results of serial exercise treadmill testing. Thus, no early adverse effects of acute nifedipine withdrawal were found in patients with prior rest angina at the time of bypass surgery or in stable patients receiving long-term medical therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Regional wall motion improvement after coronary thrombolysis with recombinant tissue plasminogen activator: importance of coronary angioplasty.

To evaluate functional recovery in 20 consecutive patients with acute myocardial infarction who received recombinant tissue-type plasminogen activator, serial two-dimensional echocardiograms were performed before and immediately after tissue plasminogen activator administration and at 1 and 10 days postinfarction. Tissue plasminogen activator was administered intravenously (17 patients) or by intracoronary infusion (3 patients) after angiographic confirmation of total occlusion. Reperfusion, documented by angiography, occurred in 13 of the 20 patients. The mean time from onset of chest pain to thrombolysis was 5.1 +/- 1.1 hours. Echocardiograms were evaluated for regional function with a visual semiquantitative scoring system by two independent observers who had no knowledge of patient identity, temporal sequence, therapy or effect of therapy. There was no immediate or 24 hour improvement in wall motion. At day 10 compared with pretreatment, 28 of 33 reperfused infarct zone segments versus 6 of 20 nonreperfused infarct segments demonstrated improved wall motion (p = 0.01). This improvement did not relate to time from onset of chest pain to successful thrombolysis. Of reperfused infarct zone segments in the distribution of coronary artery balloon dilation, 19 of 23 segments exhibited improvement versus 7 of 17 (reperfused, no angioplasty) and 6 of 20 (nonreperfused, no angioplasty) segments (p = 0.001). Infarct zone segments reperfused at the time of ongoing chest pain demonstrated functional recovery compared with segments reperfused in the absence of chest pain (18 of 23 versus 10 of 20, respectively; p = 0.05). Thus, in this uncontrolled series, there was echocardiographically detectable improvement in function of reperfused infarct segments 10 days after coronary thrombolysis with recombinant tissue plasminogen activator.

Therapeutic choices in unstable angina.

Unstable angina pectoris is a high-risk ischemic syndrome with complex, interacting pathophysiologic mechanisms that include coronary atherosclerosis, coronary vasoconstriction, and thrombosis. The roles of various medical strategies, including nitrates, beta blockers, calcium antagonists, and antiplatelet, anticoagulant, and thrombolytic agents, are discussed in conjunction with revascularization procedures such as coronary angioplasty and bypass surgery.

Assessing the total ischemic burden in the management of unstable angina. A review.

Unstable angina is a common ischemic syndrome that is characterized by chest pain occurring at rest often with transient ischemic electrocardiographic changes. Although most patients with unstable angina experience relief of pain with intensive medical therapy while in the coronary care unit, they subsequently have a high incidence of unfavorable cardiac events usually occurring within several months. Continuous electrocardiographic monitoring for ischemia has demonstrated a relatively high incidence of ischemic episodes both in patients with stable and unstable angina pectoris. The prognostic importance of such findings has been previously uncertain. The prognostic significance of silent myocardial ischemia in patients with unstable angina receiving intensive medical therapy has been addressed in a study of hospitalized patients in a coronary care unit. All patients were treated with nitrates, nifedipine, and propranolol. Continuous two-channel electrocardiographic monitoring was performed during the first two days of medical therapy. The electrocardiographic recordings were interpreted blindly for frequency and duration of ischemic changes, and these episodes were determined to be either symptomatic or silent. The prevalence of silent ischemic episodes, their prognostic significance, their contribution to the total ischemic burden, and the effects of different medical regimens on these variables are discussed.

Assessment of early post-infarction ischemia: correlation between ambulatory electrocardiographic monitoring and exercise treadmill testing.

PURPOSE: Demand-related myocardial ischemia detected by treadmill testing is commonly used to identify high-risk patients after myocardial infarction (MI). Although ischemia detected by ambulatory electrocardiographic monitoring (AECG) has also been shown to predict poor outcome in some patient groups, the relationship between AECG-detected ischemic ST changes and post-MI treadmill ischemia is unknown. PATIENTS AND METHODS: We screened 94 patients after MI with 24-hour AECG monitoring and a Naughton treadmill test. Forty-two patients were excluded because of left bundle branch block, left ventricular hypertrophy, abnormal baseline ST segments, or digoxin therapy. In the remaining 52 patients, AECG was performed 5.1 +/- 2.2 days after MI (mean +/- SD) and the treadmill test 8.4 +/- 2.2 days after MI. Each patient was taking the same drugs for both studies, had no interim revascularization procedures, and all studies were interpreted blindly. RESULTS: The treadmill test (ETT) was positive for ST changes and/or thallium reperfusion defects in 19 of 52 patients (36%). The AECG was positive for ischemia (ST depression greater than 1 mm, for more than 1 minute) in 14 of 52 patients (27%) (Group I), with 9.9 +/- 8.2 ischemic episodes per patient lasting 13.5 +/- 7.5 minutes per episode. The AECG was negative for ischemia in the remaining 38 patients (73%) (Group II). The ETT and AECG correlation was as follows: 9 patients with AECG-detected ischemic ST changes had positive ETT results; 10 patients without AECG-detected ischemic ST changes had positive ETT results; 5 patients with AECG-detected ischemic ST changes had negative ETT results; and 28 patients without AECG-detected ischemic ST changes had negative ETT results (p < 0.02 by chi 2). The predictive accuracy of a positive AECG identifying a positive ETT was 65% (specificity 85%, sensitivity 47%), and the predictive accuracy of a negative AECG identifying a negative ETT was 74%. Group I patients were older than Group II patients (63.6 +/- 8.2 years versus 53.2 +/- 10.6 years p < 0.02), more commonly had painless ETT ischemia (43% versus 18% p = 0.08), and tended to have positive ETT results at a lower level of exercise (366 +/- 210 seconds versus 588 +/- 212 seconds, p = 0.04). CONCLUSION: Ischemic ST changes as detected by AECG monitoring correlate significantly with post-MI treadmill test results with a high specificity, albeit a low sensitivity. In patients without baseline ST-segment abnormalities and limited exercise capability, AECG monitoring may be of limited use in identifying early post-MI ischemia.

Association between silent myocardial ischemia and prognosis: insensitivity of angina pectoris as a marker of coronary artery disease activity.

The clinical syndrome of angina pectoris was accurately described over 200 years ago by Sir William Heberden. However, in recent years, we have learned that many episodes of myocardial ischemia occur that are not accompanied by symptoms of angina pectoris. These silent ischemic episodes may be detected either during exercise testing, using electrocardiographic criteria that can be combined with scintigraphic studies evaluating myocardial blood flow (thallium perfusion studies) or left ventricular function (gated blood pool scans). In addition, continuous electrocardiographic (Holter) monitoring can be used for the detection of transient ST-segment changes; these changes on Holter monitoring have been correlated with abnormalities of myocardial perfusion and function, indicating that they represent true ischemic events. Studies have shown that patients with coronary artery disease who have evidence of ongoing ischemia, whether symptomatic or silent, have an increased risk for experiencing subsequent cardiac events than patients without evidence of ischemia. Many studies have demonstrated that ischemia during an exercise study after myocardial infarction identifies patients at high risk for recurrent cardiac events, whether or not the ischemia is associated with angina pectoris. Holter monitoring has allowed for the detection of ischemic events out of hospital in ambulatory patients. Studies in stable angina patients have shown that there are many asymptomatic episodes in this setting, which are often occurring at low heart rates during activities of everyday life, without an apparent significant increase in myocardial oxygen demands, and these episodes may even be precipitated by mental stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Safety of acute calcium antagonist withdrawal: studies in patients with unstable angina withdrawn from nifedipine.

The acute effects of nifedipine withdrawal were studied in 81 patients with angina at rest who had completed a prospective, double-blind, randomized trial of nifedipine versus placebo. Thirty-nine of the 81 patients (group 1) were withdrawn from nifedipine or placebo at the time of coronary artery bypass surgery for uncontrolled angina or left main coronary artery disease. When the patients withdrawn from nifedipine were compared with those withdrawn from placebo, no significant differences were seen in the incidence of hypotension, myocardial infarction, significant arrhythmias or vasopressor or vasodilator requirements during the perioperative period. Forty-two patients (group 2) completed 2 years on a protocol consisting of nitrates and propranolol, in addition to nifedipine or placebo. These patients were hospitalized for a controlled withdrawal of the study drug (nifedipine or placebo), and no significant difference was noted in either exercise performance on serial treadmill testing or the number or duration of episodes of ischemic ST-segment changes during continuous electrocardiographic monitoring. Eight patients continued to experience occasional episodes of angina at rest. Angina at rest recurred during the withdrawal period in 5 of these 8 patients. Four of these 5 patients were withdrawn from nifedipine. Of the 34 stable patients in group 2 who were not experiencing angina at rest before withdrawal, none had angina at rest during the withdrawal study period. Thus, there were no early untoward effects of acute nifedipine withdrawal either in patients undergoing coronary bypass surgery or in stable patients on long-term medical therapy. However, patients with persistent symptoms of angina at rest may experience early recurrent ischemia upon withdrawal from nifedipine.

Thrombolysis in postinfarction angina.

Postinfarction angina carries a poor prognosis, with a 20-70% incidence of recurrent myocardial infarction (MI) or death within the subsequent 3-6 months. The pathophysiologic mechanisms causing postinfarction angina may include thrombus, complex coronary arterial lesions that form a nidus for thrombus formation, inadequate collateral supply following acute MI, or intimal endothelial dysfunction. The role of thrombus has been established in the pathophysiology of Q-wave MI, and thrombolytic treatment of patients presenting with acute transmural MI has been shown to salvage left ventricular function and to reduce mortality. However, thrombolytic therapy for the acute MI does not reduce the incidence of recurrent ischemia or infarction, as is evident from the 18-26% incidence of recurrent ischemia reported in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) and Thrombolysis in Myocardial Infarction (TIMI) trials. In the Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI) study the incidence of reinfarction was documented as 4% in the streptokinase group, which was actually significantly greater than in the placebo group (2%). In a randomized placebo-controlled study of thrombolysis for postinfarction angina, 29 patients were randomized to placebo (P group, n = 17) or to thrombolytic therapy (T group, n = 12). Patient groups were similar with respect to age, location of MI, ejection fraction, severity of coronary artery disease, and antianginal therapy. Patients underwent coronary angiography 6 +/- 1 days postinfarction. Filling defects consistent with intracoronary thrombus was seen in 11 of 12 T group patients and in 11 of 17 P group patients prior to treatment. Lysis occurred in 7 of 11 T patients and 1 of 11 P (p less than 0.02). Holter-detected silent ischemia was compared pre- and posttherapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Frequency and importance of silent myocardial ischemia identified with ambulatory electrocardiographic monitoring in the early in-hospital period after acute myocardial infarction.

The incidence and clinical significance of silent myocardial ischemia occurring in the early period after acute myocardial infarction (AMI) was studied in 59 patients who had an uncomplicated early course after admission for AMI. Calibrated 2-lead ambulatory electrocardiographic monitoring performed for 39 +/- 2 hours starting 4 +/- 1 days after AMI identified silent myocardial ischemia, defined as greater than or equal to 1 mm ST-segment change lasting greater than or equal to 2 minutes, in 27 patients. These patients had 5 +/- 1 episodes lasting a median of 11 minutes/episode (range 2 to 36 minutes/episode). Patients with and without silent ischemia had comparable baseline demographics, were receiving similar anti-ischemic medications and had similar severity of coronary disease by angiography. No reinfarctions occurred during the in-hospital period. Fourteen of 27 patients (52%) with silent ischemia had greater than or equal to 1 in-hospital clinical ischemic event (pulmonary edema, n = 5, cardiac death, n = 1, and postinfarction angina, n = 11). In contrast, only 7 of 32 patients without silent ischemia (22%) had greater than or equal to 1 in-hospital event (pulmonary edema, n = 1, cardiac death, n = 1, and postinfarction angina, n = 6). The frequency of ischemic events was significantly greater in patients with silent ischemia compared to those without silent ischemia, p less than 0.02. Silent ischemia occurs frequently very early after AMI and identifies a group of patients who are at increased risk for adverse in-hospital clinical outcomes.

Death after acute myocardial infarction: interrelation between left ventricular dysfunction, arrhythmias and ischemia.

Patients who survive an acute myocardial infarction face an increased risk of sudden death for approximately 6 months after hospital discharge; their prognosis is determined by the severity of their coronary arteriosclerosis and the degree of left ventricular dysfunction. Frequent ventricular premature complexes and evidence of ischemia either spontaneously or on treadmill are also markers for early morbidity and mortality in patients who are discharged from the hospital after acute myocardial infarction. The degree of left ventricular dysfunction is the strongest predictor of mortality; patients who have both left ventricular dysfunction, frequent premature ventricular beats and evidence of ischemia are at the highest risk of mortality after hospital discharge. It appears likely that all 3 of these risk factors interact and that therapy to reduce morbidity and mortality after myocardial infarction should aim at the amelioration of each of these risk factors. A model for the interaction of these risk factors is proposed and an approach to treatment for patients at high risk of mortality after hospital discharge after myocardial infarction is suggested.

Intracoronary thrombolysis 3 to 13 days after acute myocardial infarction for postinfarction angina pectoris.

The restoration of anterograde coronary flow long after coronary thrombosis may be of benefit to patients with continuing ischemia. To determine whether "old" intracoronary thrombi are susceptible to lysis with thrombolytic agents, 18 patients with angina at rest during evolving acute myocardial infarction (AMI) and total occlusion of the infarct vessel were treated with intracoronary streptokinase 3 to 13 days after onset of AMI. In 12 of the 18 patients (67%), successful recanalization of the artery was achieved 6.9 +/- 2.7 days after AMI. Thrombolysis was followed by coronary angioplasty in 2 patients. To evaluate the efficacy of this approach in reducing post-AMI ischemia, the number of episodes of angina at rest was compared in patients with successful and unsuccessful attempts at recanalization. Even in patients without angioplasty, the mean number of daily episodes decreased from 1.02 +/- 0.6 to 0.09 +/- 0.2 in patients in whom reperfusion was achieved, and from 1.07 +/- 0.8 to 0.88 +/- 0.8 in those in whom it was not (p = 0.027 for the difference between the groups). Thus, in patients with early post-AMI angina, intracoronary streptokinase can restore flow in the occluded artery, may decrease the frequency of angina, and allows angioplasty to be performed.

Frequency and significance of early postoperative silent myocardial ischemia in patients having peripheral vascular surgery.

Coronary disease causes the majority of perioperative complications after peripheral vascular surgery. Twenty-four patients with stable coronary disease undergoing peripheral revascularization were studied using continuous electrocardiographic monitoring to determine the incidence of perioperative asymptomatic myocardial ischemia and its relation to postoperative clinical ischemic events. Patients were monitored preoperatively (17 +/- 1 hours), intraoperatively and postoperatively (29 +/- 2 hours) using 4-channel calibrated amplitude-modulated units. Fifteen patients (63%) had early postoperative silent ischemia; 3 also had preoperative silent ischemia and 5 intraoperative transient ischemia. Patients with and without silent ischemia had similar clinical characteristics, perioperative antianginal medications and postoperative episodes of hemodynamic instability. However, 8 of 15 patients (53%) with silent ischemia had postoperative clinical ischemic events (2 had myocardial infarction, 2 had new congestive heart failure and 4 had new rest angina), versus only 1 of 9 patients (11%) without silent ischemia who had angina (p less than 0.05). Early postoperative silent myocardial ischemia occurs frequently after vascular surgery and is associated with postoperative clinical ischemic events.

Incremental reduction of serum total cholesterol and low-density lipoprotein cholesterol with the addition of plant stanol ester-containing spread to statin therapy.

This study compares the effect of plant stanol ester spread with a placebo spread on cholesterol in patients taking statin therapy, but who still had elevated low-density lipoprotein (LDL) cholesterol. This was a randomized, double-blind, placebo-controlled clinical trial, with 67 women and 100 men with LDL cholesterol >/=130 mg/dl and triglycerides

An angiographic and functional comparison of patients with silent and symptomatic treadmill ischemia early after myocardial infarction.

Sixty consecutive patients were studied who had positive responses to Naughton exercise treadmill testing (at least 1.5 mm of ST-segment shift in at least 2 leads or thallium reperfusion abnormalities) with or without symptoms of angina 11 +/- 1 days after acute myocardial infarction (AMI). All patients had undergone coronary angiography 24 +/- 4 days after infarction. Thirty-eight patients (63%) had no treadmill angina (silent ischemia, group I) and 22 patients had typical treadmill angina (symptomatic ischemia, group II). Use of beta-blocking drugs, calcium antagonists and nitrates at the time of exercise testing did not differ in the 2 groups. All 9 patients with diabetes mellitus were in the asymptomatic group (p less than 0.40) and group I had a greater proportion of inferior wall AMI (30 of 38) than group II (11 of 22, p = 0.02). Total exercise treadmill test duration (group I 422 +/- 31 seconds, group II 400 +/- 46 seconds) and rate-pressure product were not different in the 2 groups. The number of patients unable to exercise 5 minutes (12 in group I and 7 in group II), the number with diffuse electrocardiographic changes (9 in group I and 7 in group II), and the number with inadequate blood pressure response (8 in group I and 4 in group II) were also similar. At coronary arteriography the mean number of arteries with at least 70% diameter stenosis was 2.0 +/- 0.2 in group I and 2.2 +/- 0.2 in group II (difference not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Identification of patients at high risk for complications of intraaortic balloon counterpulsation: a multivariate risk factor analysis.

Risk factors for vascular complications of intraaortic balloon (IAB) counterpulsation were evaluated in 206 consecutive patients. The approach was percutaneous in 105 patients and surgical cutdown in 101. Vascular complications occurred in 42 patients, and of these 21 required surgery. Multivariate analysis demonstrated the following major risk factors for vascular complications: preexisting peripheral vascular disease (PVD) defined as a history of claudication, femoral bruit or absent pedal pulse (p less than 0.01); and the use of the percutaneous approach (p = 0.02). Evidence of PVD was particularly predictive of major vascular complications requiring surgery (p less than 0.01). In patients with evidence of previous PVD, the risk for a major vascular complication was 31% with the percutaneous, and 16% with the surgical cutdown approach. Without PVD, the risk for a major vascular complication was 4 times higher in women (15%) than in men (3.5%), but in the presence of PVD gender had no significant effect (p = 0.03). Age, duration of IAB counterpulsation and indication for insertion were not significant risk factors. It is concluded that (1) without previous PVD, women are at greater risk than men for major vascular complications (due to smaller arterial size); and (2) evidence of previous PVD identifies patients at high risk for major vascular complications with IAB counterpulsation, particularly by way of the percutaneous approach.

Effects of carbon monoxide on myocardial ischemia.

The purpose of this study was to determine whether low doses of carbon monoxide (CO) exacerbate myocardial ischemia during a progressive exercise test. The effect of CO exposure was evaluated using the objective measure of time to development of electrocardiographic changes indicative of ischemia and the subjective measure of time to onset of angina. Sixty-three male subjects (41-75 years) with well-documented coronary artery disease, who had exertional angina pectoris and ischemic ST-segment changes in their electrocardiograms, were studied. Results from three randomized, double-blind test visits (room air, low and high CO) were compared. The effect of CO exposure was determined from the percent difference in the end points obtained on exercise tests performed before and after a 1-hr exposure to room air or CO. The exposures resulted in postexercise carboxyhemoglobin (COHb) levels of 0.6% +/- 0.3%, 2.0% +/- 0.1%, and 3.9% +/- 0.1%. The results obtained on the 2%-COHb day and 3.9%-COHb day were compared to those on the room air day. There were 5.1% (p = 0.01) and 12.1% (p less than or equal to 0.0001) decreases in the time to development of ischemic ST-segment changes after exposures producing 2.0 and 3.9% COHb, respectively, compared to the control day. In addition, there were 4.2% (p = 0.027) and 7.1% (p = 0.002) decreases in time to the onset of angina after exposures producing 2.0 and 3.9% COHb, respectively, compared to the control day. A significant dose-response relationship was found for the individual differences in the time to ST end point and angina for the pre- versus postexposure exercise tests at the three carboxyhemoglobin levels. These findings demonstrate that low doses of CO produce significant effects on cardiac function during exercise in subjects with coronary artery disease.

Double vs single balloon technique for aortic balloon valvuloplasty.

Percutaneous aortic valvuloplasty using a single dilating balloon has been associated with significant but modest reduction in transvalvular pressure gradient and increase in valve area. The balloon diameter is usually 20 mm or smaller to avoid disruption of aortic root structure and to permit forward blood flow during inflation. To evaluate the safety and efficacy of valvuloplasty using a combination of balloons with larger maximum inflated diameters, we compared results of aortic valvuloplasty in 21 patients using either the single or double balloon technique. Mean maximum inflated balloon diameter was 19.4 mm +/- 1.4 for the single balloon technique, while the mean sum of diameters for the simultaneous double balloon technique was 36.3 mm +/- 3.9. The mean age, aortic annulus diameter, and predilatation aortic valve area were not different among groups. Mean aortic transvalvular gradient reduction and mean aortic valve area increase were greater for the double balloon technique. The procedure was well tolerated with no major complications. No change in the degree of aortic regurgitation was noted. The double balloon technique for aortic valvuloplasty is safe and more effective at improving aortic valve area and transvalvular gradient than the conventional single balloon technique.