Antecedent Angina Research Articles

A CASE OF VENTRICULAR SEPTAL RUPTURE AFTER ACUTE MYOCARDIAL INFARCTION

When ventricular septal rupture (VSR) complicates acute myocardial infarction the mortality is usually high. Reperfusion therapy has reduced its incidence. However if VSR has developed then rapid diagnosis, aggressive medical management, and surgical intervention are required to optimize recovery and survival. In the era before reperfusion therapy, septal rupture complicated 1 to 3 percent of acute myocardial infarctions. Among the 41,021 patients in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial, ventricular septal rupture was suspected in 140 patients (0.34 percent) and confirmed by a retrospective review in 84 (0.2 percent). Thus, reperfusion therapy has decreased the incidence of septal rupture. Septal rupture occurs more frequently with anterior wall acute myocardial infarction than other types of acute myocardial infarction. Risk factors for septal rupture included hypertension, advanced age (60 to 69 years), female sex and the absence of a history of angina or myocardial infarction. Angina or previous infarction may lead to myocardial preconditioning as well as to the development of coronary collaterals, both of which reduce the likelihood of septal rupture. In patients undergoing thrombolysis advanced age, female sex, and the absence of smoking are often associated with an increased risk of septal rupture, whereas the absence of antecedent angina has not been associated with an increased risk. In the GUSTO-I trial, there was a nonlinear relation between the systolic and diastolic blood pressures at enrolment and septal rupture, since hypertension and extensive myocardial infarction and right ventricular infarction are also risk factors for septal rupture

Analysis of risk factors of ST-segment elevation myocardial infarction in young patients.

BackgroundAcute myocardial infarction (AMI) is often present in old populations and rare in young people. Its incidence significantly increased recent years. The mechanism and disease course of AMI in young people are probably different from that in old population. The aim of this study was to analyze clinical risk factors of STEMI in young patients.MethodsData was collected from consecutive patients ≤ 44 years of age (young; n = 86) and 60–74 years of age (old; n = 65) diagnosed with STEMI, and 79 young age-matched patients without coronary artery disease (CAD), hospitalized between January 2009 and June 2013.ResultsThe young STEMI group had a significantly higher proportion of males (88.37 vs. 53.16%; P < 0.01), smokers (82.56 vs. 49.37%; P < 0.01) and patients with a family history of early CAD (54.65 vs. 32.91%; P < 0.05) than age-matched controls. Young STEMI patients also had significantly higher levels of fasting blood sugar (6.39 vs. 5.25 mmol/L; P < 0.001), glycated hemoglobin (HbA1c) (6.26 vs. 5.45%; P < 0.05), total cholesterol (5.14 vs. 4.65 mmol/L, P < 0.05), and fibrinogen (Fib) (3.39 vs. 2.87; P < 0.01). Compared with the old STEMI group, young STEMI patients had significantly higher proportions of males (88.37 vs. 63.08%; P < 0.01) smokers (82.56 vs. 41.54%; P < 0.01), and those with a family history of early CAD (54.65 vs. 18.46%; P < 0.01). Young STEMI patients also lower Fib (3.39 vs. 3.88 g/L; P < 0.01), less frequent occurrence of angina pectoris before STEMI (13.95 vs. 29.23%; P < 0.05) compared with the old STEMI group. Logistic regression analysis indicated that male sex (OR = 5.891), smoking (OR = 3.500), family history of early CAD (OR = 3.194), Fib (OR = 2.414) and HbA1c (OR = 1.515) are associated with STEMI in young patients.ConclusionIn addition to previously recognized risk factors (male sex, smoking and family history of early CAD), Fib and HbA1c are associated with STEMI in individuals ≤ 44 years of age without antecedent angina pectoris.

Exogenous adenosine triphosphate disodium administration during primary percutaneous coronary intervention reduces no-reflow and preserves left ventricular function in patients with acute anterior myocardial infarction: A study using myocardial contrast echocardiography

Background It is unknown whether adenosine triphosphate disodium (ATP) administration during primary percutaneous coronary intervention (PCI) is useful in anterior acute myocardial infarction (AMI). Methods The study was a prospective, non-randomized, open-label trial. Primary PCI was successfully performed in 204 consecutive patients with first anterior AMI. ATP at a mean dose of 117 μg/kg/min for 45 min on an average was infused intravenously during PCI in 100 patients (Group 1). In the other 104 patients, normal saline was administered (Group 2). ST-segment resolution (STR) was estimated 90 min after recanalization. The no-reflow ratio was measured 2 weeks later, using intravenous myocardial contrast echocardiography. Left ventricular ejection fraction (LVEF), LV regional wall motion (LVRWM), and LV end-diastolic volume index (LVEDVI) were measured 6 months later. Results Baseline patient characteristics of the two groups were similar, including TIMI risk scores. Significant STR (≧ 50% resolution compared to baseline) (66% versus 50%; Group 1 versus Group 2, p = 0.02), no-reflow ratio (24% versus 34%, indicated by mean values, p = 0.02), LVEF (61% versus 55%, p = 0.0007), LVRWM (− 1.56 versus − 2.05, using the SD/chord, p = 0.0001), and LVEDVI (60 ml/m 2 versus 71 ml/m 2, p = 0.0007) were significantly better in Group 1, and the no-reflow ratio, LVEF, LVRWM and LVEDVI were significantly better in ATP-administered patients, regardless of antecedent angina or advanced age. ATP Administration was consistently identified as a significant determinant for STR, no-reflow ratio, LVEF, LVRWM, and LVEDVI. Conclusions Intravenous ATP administration during reperfusion is an independent determinant of STR and the no-reflow ratio, and LVEF, LVRWM, and LVEDVI at 6 months after primary PCI.

S33-1 PREINFARCTION ANGINA ASSOCIATES WITH ABSENCE OF RIGHT VENTRICULAR INFARCTION AFTER FIRST ACUTE INFERIOR MYOCARDIAL INFARCTION

Objective: We sought to examine the association between preinfarction angina and a lower risk of right ventricular infarction (RVMI) in patients with first acute inferior myocardial infarction (MI). Methods: One hundred seventy patients who were admitted to cardiac care unit after first acute inferior MI with ST segment elevation and symptom duration < 12 hours and received thrombolysis were studied. Preinfarction angina within 24 hours prior to MI was present in 62 patients (Angina group) whereas the remaining 108 patients (Cohort group) had no chest pain preceding acute MI. The course of the inhospital phase of MI was analyzed. The outcomes studied were presence of RVMI together with inferior MI, major complications and in-hospital mortality. Results: In angina group 15 (24.2%) patients had RVMI, while in control group 70 (64.8%) patients suffered from RVMI (adjusted odds ratio‚0.32%, confidence interval‚0.09 to 0.86 P=0.01). Absence of preinfarction angina was predictor of development of RVMI (P< 0.001)‚ complete atrioventricular block; (P< 0.01)‚ cardiogenic shock (P< 0.001) and in-hospital mortality (P = 0.02). Conclusion: Patients with Preinfarction angina‚ occurring within 24 hours of acute MI‚ have a lower rate of right ventricular infarction and better in-hospital outcome than patient without antecedent angina. These results may be attributed to the protective effects of ischemic preconditioning. (Rawal Med J 2008;33:43-46).

The Evolving Pattern of Symptomatic Coronary Artery Disease in the United States and Canada: Baseline Characteristics of the Clinical Outcomes Utilizing Revascularization and Aggressive DruG Evaluation (COURAGE) Trial

Major improvements in medical therapy and percutaneous coronary intervention for coronary artery disease (CAD) have emerged during the previous 2 decades, but no randomized trial in patients with stable CAD has been powered to compare these 2 strategies for the hard clinical end points of death or myocardial infarction (MI), and previous studies have not evaluated the effect of coronary stents and intensive medical therapy on cardiac events during long-term follow-up. Between 1999 and 2004, 2,287 patients with documented myocardial ischemia and angiographically confirmed CAD were randomized to the Clinical Outcomes Utilizing Revascularization and Aggressive DruG Evaluation (COURAGE) trial, with a principal hypothesis that a strategy of percutaneous coronary intervention plus intensive, guideline-driven medical therapy would be superior to a strategy of intensive medical therapy alone. The primary end point was a composite of all-cause mortality or acute MI (time to first event) during a 2.5- to 7-year (median 5) follow-up. Baseline characteristics were a mean age of 62 +/- 5 years, 85% men, and 86% Caucasian. Mean duration of angina before randomization was 26 months (average 10 episodes/week), and 29% of patients were smokers, 67% had hypertension, 38% had previous MI, 71% had dyslipidemia, 34% had diabetes, 27% had previous revascularization, and 69% had multivessel CAD. Approximately 55% of patients met established criteria for the metabolic syndrome. In conclusion, baseline characteristics of the COURAGE trial study population indicate a highly symptomatic group of patients with CAD who have a significant duration and frequency of antecedent angina pectoris and a high prevalence of cardiac risk factors.

Comparison of clinical and angiographic features and longterm follow-up events between patients with variant angina and patients with ST elevation myocardial infarction

We investigated to what extent patients with variant angina and significant coronary stenosis (≥ 70%) present a clinical and angiographic profile similar to patients with ST elevation myocardial infarction. Thus, the clinical and angiographic features as well as follow-up events of 200 patients were prospectively analyzed and were compared with those of 422 patients with a first ST elevation myocardial infarction survivors of the early phase (3 days) and those of 70 patients with variant angina and non significant stenosis. Age and incidence of smoking, systemic hypertension, diabetes and maximum ST elevation were similar in the 2 groups. Furthermore, among patients with significant coronary stenosis, stenosis severity and the proportion of eccentric lesions were also comparable. Incidence of recent–within 30 days prior to admission–angina at rest was higher in variant angina patients with significant stenosis (67% vs. 27%, p < 0.001) than in those with myocardial infarction but long standing angina at rest (> 30 days) was low and comparable in these 2 groups (15% vs. 11%, ns). Also, in a 5-year follow-up most patients from these 2 groups were free from angina at rest (86% vs. 84%) which in variant angina patients was largely attributable to a high revascularization rate (72%). Moreover, the rate of myocardial infarction/cardiac death (20% vs. 19%) was also similar. Patients with variant angina and non-significant stenosis, however, had longer antecedent angina, more frequent follow-up angina and a lower incidence of cardiac events than the other 2 groups. Thus, these findings suggest that patients with variant angina and significant coronary stenosis generally behave as an acute coronary syndrome–likely associated with an acutely complicated plaque–rather than as recurrent vasospastic angina, and should be managed accordingly.

Prevalence and distribution of coronary disease in claudicants using 12-lead precordial stress electrocardiography

Aims: to evaluate the prevalence of coronary artery disease (CAD) by means of modified stress electrocardiography in patients presenting with intermittent claudication. Methods: three hundred consecutive patients (188 male) with intermittent claudication (post-exercise ankle brachial index <0.8), and 100 age and sex-matched controls, were assessed for CAD with resting and stress 12-lead-precordial ECG. A history of angina and previous myocardial infarction (MI) was recorded. Exclusion criteria: recent (<1 month) MI; unstable angina; prior coronary intervention; arrhythmias; conduction abnormalities; uncontrolled hypertension; heart failure, digoxin therapy, and inability to perform tests. Results: based on antecedent angina, MI and abnormal resting ECG, CAD prevalence was 47% in claudicants and 6% in controls; on 12-lead-precordial ECG stress testing, CAD prevalence was 46% (95% CI: 40.1-51.7%) in claudicants and 11% (95% CI: 4.8-17.2%) in controls (both p < 0.0001). Only 67% of claudicants (n = 141) with antecedent angina, MI or an abnormal resting ECG, met the criteria of CAD on stress testing; also 28% of claudicants without antecedent angina, MI and a normal resting ECG (n = 159) had evidence of CAD. The odds ratio for CAD in claudicants was 6.9. Based on 12-lead-precordial ECG stress testing we detected the presence of: one-, two- and three-vessel disease in 14.7% (95% CI: 10.6-18.7%), 19% (95% CI: 14.5-23.5%) and in 12.3% (95% CI: 8.6-16%) of claudicants; and in 8, 3 and 0% of controls, respectively. Conclusions: forty six percent of patients with intermittent claudication had concomitant CAD, and 31% two- or three- vessel disease. In the presence of claudication the odds ratio for CAD is 6.9 (95% CI: 3.5-13.4) and for two- or three-vessel disease 14.8. Non-invasive modified stress electrocardiography by enabling identification of those with multi-vessel CAD and thus by providing cardiac risk stratification may help bridge the gap between clinical evaluation and invasive coronary imaging.Eur J Vasc Endovasc Surg 25, 519-526 (2003)

Evidence of a cellular protective effect by antecedent angina independent of collateral flow recruitment during coronary angioplasty in humans.

The main aim of this study was to elucidate whether the beneficial effect of antecedent angina is a cellular protective effect or the result of an increase of collateral flow. Of 42 patients with angina who underwent percutaneous transluminal coronary angioplasty (PTCA) for proximal left anterior descending artery (LAD) stenosis, 22 had experienced antecedent anginal pain (AP) within 7 days prior to PTCA. 99mTc-sestamibi was injected during balloon inflation, and quantitative analysis of ischemic severity during coronary occlusion was calculated (SS). An electrocardiogram was recorded during ballooning to calculate the sum of ST elevation (sumST). SumST was significantly reduced in patients with AP compared with patients without AP (1.88+/-0.89 mV vs 1.18+/-0.74 mV, p=0.0088); however, no difference was observed in defect severity. A close correlation was observed between SS and sumST in both groups. The multivariate regression model demonstrated that both a large SS (p<0.0001) and the absence of preceding AP (p=0.001) were significantly related to the elevation of sumST. Recent angina can render the myocardium more resistant to subsequent ischemia during angioplasty and is true preconditioning rather than simply an increase of flow.

Optimal time for predicting myocardial viability after successful primary angioplasty in acute myocardial infarction: a study using myocardial contrast echocardiography

This study sought to elucidate serial changes in microvascular integrity during papaverine-induced hyperemia in the risk area for myocardial infarction. In addition, we attempted to determine the optimal time for predicting myocardial viability. Seventy-two patients who underwent serial myocardial contrast echocardiography (MCE) before and shortly after (day 1), 1 day (day 2), and 3 weeks (day 21) after recanalization were studied. In 18 of 72 patients, MCE was performed at baseline and during hyperemia using selective intracoronary infusion of papaverine. Both the peak gray-scale ratio (PGSR) within the risk area, and the no- and low-reflow ratio (LR ratio) were analyzed in each stage. Left ventricular regional wall motion (RWM) was determined 6 months after recanalization. The correlation coefficient between PGSR with papaverine on day 1 and that on day 2 was 0.54 (p = 0.02); it was 0.50 (p = 0.04) between day 1 and day 21, and 0.82 (p = 0.001) between day 2 and day 21. On day 1, the correlation coefficient between the LR ratio with papaverine and RWM was 0.60 (p = 0.02), which changed to 0.72 (p = 0.003) on day 2 and 0.54 (p = 0.04) on day 21, respectively. The best time to predict viable myocardium was established on day 2 by receiver operating characteristics curves. ST-segment re-elevation, elapsed time from onset to recanalization, and antecedent angina pectoris were independent factors for PGSR on day 2 using stepwise and multiple linear regression analysis. This study suggests that the optimal time to estimate microvascular integrity for predicting myocardial viability might be 1 day after recanalization, which is neither shortly after recanalization nor during the convalescent stage.

Limitations of spontaneous reperfusion and conventional medical therapy to afford myocardial protection through antecedent angina pectoris in acute myocardial infarction.

Despite the cardioprotective effect of rapid coronary reperfusion, the effects of spontaneous recanalization on myocardial viability and metabolism are unknown. We studied whether preinfarction angina affords cardioprotection when spontaneous coronary reperfusion occurred in acute infarct patients. Myocardial tomographies with thallium and I-123-labeled-beta-methyl-p-iodophenyl penta-decanoic acid (BMIPP) were performed in 27 acute myocardial infarct patients treated medically: 15 patients had preexisting angina before infarction (group A) and 12 did not (group B). Thallium and BMIPP abnormalities and regional function were quantified by a polar map and contrast ventriculography, respectively. There was no significant difference between thallium and BMIPP in the severity index in groups A and B (89 +/- 97 vs. 85 +/- 68, 97 +/- 28 vs. 95 +/- 27, respectively), and no significant difference between the groups in the thallium or BMIPP severity index. The ratio of the thallium severity index to that of BMIPP and the regional wall-motion abnormality index were identical in groups A and B. Both patient groups were divided into 2 subgroups based on the presence or absence of spontaneous coronary reperfusion: subgroups A1 and A2, and subgroups B1 and B2, respectively. There were no significant differences among the 4 subgroups in severity indexes for both tracers, the thallium/BMIPP ratio, or the asynergy score. The BMIPP severity index correlated significantly with that of thallium in all subgroups, but no significant difference between the regression lines was found. It is therefore unlikely that spontaneous coronary recanalization affords beneficial effects through preservation of myocardial viability in an ischemia-related zone, suggesting that the cardioprotective effect of preinfarction angina is a limited phenomenon in patients undergoing rapid coronary reperfusion.

Antecedent angina pectoris as a predictor of better functional and clinical outcomes in patients with an inferior wall acute myocardial infarction

We examined whether angina pectoris (AP) occurring shortly before the onset of acute myocardial infarction (AMI) can render the right ventricle and the conducting tissue resistant to ischemia in 75 patients with an inferior wall AMI. Each patient had total occlusion in the proximal right coronary artery and underwent successful coronary angioplasty ≤24 hours from the onset. We divided patients into 2 groups based on presence or absence of antecedent AP ≤24 hours before the system onset: group 1 (absent) = 57 patients; group 2 (present) = 18 patients. Collateral circulation was more frequently observed in group 2 than in group 1 (group 1 vs 2, 28% vs 61%, p <0.01). Elevation in ST segment ≥1 mm in lead V 4R, hemodynamic right ventricular dysfunction, and frequency of high-degree heart block were more frequent in group 1 than in group 2 (75% vs 44%, 79% vs 39%, 53% vs 11%, p <0.05, respectively). Multivariate analysis demonstrated that antecedent AP is the only factor related to these complications. Thus, episodes of AP occurring shortly before onset may restrain development of ischemic damage of the right ventricle and conducting tissue, and are associated with better clinical and functional outcomes among patients with an inferior wall AMI.

Preinfarction Angina and Improved Reperfusion of the Infarct-related Artery

Preinfarction angina and early reperfusion of the infarct-related artery are major determinants of reduced infarct-size in patients with acute myocardial infarction. The beneficial effects of preinfarction angina on infarct size have been attributed to the development of collateral vessels and/or to post-ischemic myocardial protection. However, recently, a relation has been found between prodromal angina, faster coronary recanalization, and smaller infarcts in patients treated with rt-PA: those with preinfarction angina showed earlier reperfusion (p = 0.006) and a 50% reduction of CKMB-estimated infarct-size (p = 0.009) compared to patients without preinfarction angina. This intriguing observation is consistent with a subsequent observation of higher coronary recanalization rates following thrombolysis in patients with prodromal preinfarction angina compared to patients without antecedent angina. Recent findings in dogs show an enhanced spontaneous lysis of platelet-rich coronary thrombi with ischemic preconditioning, which is prevented by adenosine blockade, suggesting an antithrombotic effect of ischemic metabolites. Understanding the mechanisms responsible for earlier and enhanced coronary recanalization in patients with preinfarction angina may open the way to new reperfusion strategies.

Design and Baseline Characteristics of the Veterans Affairs Non-Q-Wave Infarction Strategies In-Hospital (VANQWISH) Trial

Objectives. The Veterans Affairs Non-Q-Wave Infarction Strategies In-Hospital (VANQWISH) trial was designed to compare outcomes of patients with a non–Q wave myocardial infarction (NQMI) who were randomized prospectively to an early “invasive” strategy versus an early “conservative” strategy. The primary objective was to compare early and late outcomes between the two strategies using a combined trial end point (all-cause mortality or nonfatal infarction) during at least 1 year of follow-up.Background. Because of the widely held view that survivors of NQMI are at high risk for subsequent cardiac events, management of these patients has become more aggressive during the last decade. There is a paucity of data from controlled trials to support such an approach, however.Methods. Appropriate patients with a new NQMI were randomized to an early “invasive” strategy (routine coronary angiography followed by myocardial revascularization, if feasible) versus an early “conservative” strategy (noninvasive, predischarge stress testing with planar thallium scintigraphy and radionuclide ventriculography), where the use of coronary angiography and myocardial revascularization was guided by the development of ischemia (clinical course or results of noninvasive tests, or both).Results. A total of 920 patients were randomized (mean follow-up 23 months, range 12 to 44). The mean patient age was 61 ± 10 years; 97% were male; 38% had ST segment depression at study entry; 30% had an anterior NQMI; 54% were hypertensive; 26% had diabetes requiring insulin; 43% were current smokers; 43% had a previous acute myocardial infarction; and 45% had antecedent angina within 3 weeks of the index NQMI.Conclusions. Baseline characteristics were compatible with a moderate to high risk group of patients with an NQMI.

Ischemic Preconditioning in Unstable Coronary Syndromes: Evidence for Time Dependence

Objectives. We hypothesized a time-dependent relation between angina occurring spontaneously before percutaneous transluminal coronary angioplasty (PTCA) and the likelihood of an ischemic response during initial balloon occlusion. We further hypothesized that the ability to elicit the “classic” mode of PTCA-related preconditioning would vary with the interval from clinical angina to PTCA.Background. Antecedent angina represents a potential for myocardial preconditioning in unstable ischemic coronary syndromes.Methods. We studied 67 patients with Braunwald class III unstable coronary syndromes undergoing PTCA. The interval between the last spontaneous episode of angina preceding PTCA and initial balloon inflation was categorized as follows: 0 to 6 h; 6 to 12 h; 12 to 24 h; and >24 h.Results. Across the various intervals, there was a significant difference (p = 0.004) in the proportion of patients with an absent ischemic response during the first balloon inflation (0 to 6 h, 50%; 6 to 12 h, 35%; 12 to 24 h, 23%; and >24 h, 4%). There was, however, no difference between the first and second inflations in the proportion of patients with a diminished ischemic response until 6 to 12 h (p = 0.017) had elapsed since the last spontaneous episode of angina. Patients whose angina last occurred >24 h before the first inflation showed the greatest inducibility of PTCA-related preconditioning.Conclusions. Strong evidence exists for the occurrence of ischemic preconditioning in unstable coronary syndromes. Although the protective effect of spontaneous angina appears to wane beyond 6 h, recovery of preconditioning occurs from 6 to 12 h. Thus, preconditioning can be reinduced during PTCA with a marked potentiation of the effect at 24 h. This suggests an underlying time-dependent mechanism with a physiologic “half-life” of 6 to 12 h.

Angina-Induced Protection Against Myocardial Infarction in Adult and Elderly Patients: A Loss of Preconditioning Mechanism in the Aging Heart?

Objectives. The present study examined whether angina 48 h before myocardial infarction provides protection in adult and elderly patients.Background. The mortality rate for coronary artery disease is greater in elderly than in young patients. In experimental studies, ischemic preconditioning affords an endogenous form of protection against ischemia–reperfusion injury in adult but not in senescent hearts. Angina before myocardial infarction, a clinical equivalent of experimental ischemic preconditioning, has a protective effect in adult patients. It is not known whether angina before myocardial infarction is also protective in aged patients.Methods. We retrospectively verified whether antecedent angina within 48 h of myocardial infarction exerts a beneficial effect on in-hospital outcomes in adult (<65 years old, n = 293) and elderly (≥65 years old, n = 210) patients.Results. In-hospital death was more frequent in adult patients without than in those with previous angina (10% vs. 2.6%, p < 0.01), as were congestive heart failure or shock (10.7% vs. 3.3%, p < 0.02) and the combined end points (in-hospital death and congestive heart failure or shock) (20.7% vs. 5.9%, p < 0.0003). In contrast, the presence or absence of previous angina before acute myocardial infarction in elderly patients seems not to influence the incidence of in-hospital death (14.4% vs. 15.2%, p = 0.97), congestive heart failure or shock (11.0% vs. 11.9%, p = 0.99) and the combined end points (25.4% vs. 27.1%, p = 0.89). Logistic regression analysis models for in-hospital end points show that previous angina is a positive predictor in adult but not in elderly patients.Conclusions. The presence of angina before acute myocardial infarction seems to confer protection against in-hospital outcomes in adults; this effect seemed to be less obvious in elderly patients. This study suggests that the protection afforded by angina in adult patients may involve the occurrence of ischemic preconditioning, which seems to be lost in senescent patients.

Preconditioning

Preconditioning

Effect of angina pectoris on myocardial protection in patients with reperfused anterior wall myocardial infarction: Retrospective clinical evidence of “preconditioning”

We examined whether angina pectoris occurring shortly before the onset of acute myocardial infarction can actually preserve postischemic left ventricular function in humans. Experimental studies indicate that brief, transient episodes of ischemia render the heart very resistant to infarction from a subsequent sustained ischemic insult, an effect termed ischemic preconditioning. However, no clinical data are available concerning the implications of angina pectoris shortly before the onset of infarction in humans. We studied 84 patients with an acute anterior myocardial infarction. All patients had total occlusion of the proximal or medial portion of the left anterior descending coronary artery and achieved reflow within 6 h of onset. Patients were classified into three groups on the basis of duration of antecedent angina pectoris: group 1 = no angina (37 patients); group 2 = new angina pectoris occurring < or = 7 days of onset of infarction (22 patients); group 3 = angina pectoris beginning > 7 days before onset of infarction (25 patients). All patients underwent left ventriculography on the day of, and 28 days after, onset of infarction to determine ejection fraction and regional wall motion in the territory of the left anterior descending coronary artery by the centerline method. Angiographic collateral flow grade was higher in group 3 than in groups 1 and 2 ([mean +/- SD] group 1 = 0.08 +/- 0.7, group 2 = 0.7 +/- 0.7, group 3 = 1.5 +/- 0.8). Although there were no differences in baseline ejection fraction and regional wall motion among the three groups, the degree of improvement was significantly greater in groups 2 and 3 than in group 1 (late minus baseline ejection fraction: group 1 = 0 +/- 8%, group 2 = 7 +/- 10% group 3 = 6 +/- 10% [p < 0.05 group 1 vs. groups 2 and 3]; late minus baseline regional wall motion: group 1 = 0.2 +/- 0.4, group 2 = 0.6 +/- 0.5, group 3 = 0.5 +/- 0.6 SD/chord [p < 0.05, group 1 vs. group 2]). When the study was limited to those patients with no or poor collateral flow (31 in group 1, 19 in group 2, 10 in group 3), only group 2 patients had a significant improvement in wall motion. Angina pectoris within 24 h before onset of infarction was more frequent in group 2 (82%) than group 3 (28%, p < 0.05). Episodes of angina pectoris occurring shortly before the onset of infarction may preserve myocardial contractile function in reperfused myocardial infarction despite less support from collateral flow channels, although these are suggestive results in a limited number of patients.

Outcome of thrombolytic therapy in relation to hospital size and invasive cardiac services. The Investigators of the International Tissue Plasminogen Activator/Streptokinase Mortality Trial

The outcome of patients with acute myocardial infarction who received thrombolytic therapy was assessed in relation to the size and comprehensiveness of cardiovascular services in the admitting hospitals. Two characteristics were obtained for each of the 438 hospitals: number of beds and in-house availability of cardiovascular services (coronary catheterization laboratory and coronary angioplasty or bypass surgery). Hospitals were grouped into four categories on the basis of size (< or = 300 vs > 300 beds) and availability of cardiovascular services. Baseline and outcome variables were compared by chi 2 analysis and logistic regression. Patients were followed up for 6 months. Baseline variables were comparable among hospital categories except for significant differences in the distribution of antecedent angina and time to treatment. Significantly more coronary angioplasties and bypass surgeries were performed in patients first treated in hospitals with coronary revascularization services (4.1% and 4.2% vs 1.0% and 1.9%, P < .0001). Rates of strokes (1.9% vs 1.3% and 1.6%, P = .54), hospital mortality (11.9% vs 8.5%, (P = .11), and 6-month mortality (17.0% vs 11.8% and 12.3%, P = .03) were highest among patients treated in small hospitals that had coronary revascularization facilities. The rate of invasive procedures was higher in the smaller hospitals (odds ratio [OR], 1.44; 95% confidence limits [CL], 1.11 and 1.87; P = .006) and in hospitals with coronary revascularization services (OR, 4.05; 95% CL, 3.14 and 5.22; P < .0001); hemorrhage was more frequent in centers with coronary revascularization facilities (OR, 1.39; 95% CL, 1.13 and 1.71; P = .002). Rates of hospital mortality and 6-month mortality were similar. Patients with acute myocardial infarction treated with thrombolytic therapy have the same mortality in small centers without in-house coronary revascularization services as in larger centers with such services.

Outcome of Thrombolytic Therapy in Relation to Hospital Size and Invasive Cardiac Services

Objective: The outcome of patients with acute myocardial infarction who received thrombolytic therapy was assessed in relation to the size and comprehensiveness of cardiovascular services in the admitting hospitals. Methods: Two characteristics were obtained for each of the 438 hospitals: number of beds and in-house availability of cardiovascular services (coronary catheterization laboratory and coronary angioplasty or bypass surgery). Hospitals were grouped into four categories on the basis of size (≤300 vs >300 beds) and availability of cardiovascular services. Baseline and outcome variables were compared by χ2analysis and logistic regression. Patients were followed up for 6 months. Results: Baseline variables were comparable among hospital categories except for significant differences in the distribution of antecedent angina and time to treatment. Significantly more coronary angioplasties and bypass surgeries were performed in patients first treated in hospitals with coronary revascularization services (4.1% and 4.2% vs 1.0% and 1.9%,P Conclusions: Patients with acute myocardial infarction treated with thrombolytic therapy have the same mortality in small centers without in-house coronary revascularization services as in larger centers with such services. (Arch Intern Med. 1994;154:2237-2242)

Effect on short-term prognosis and left ventricular function of angina pectoris prior to first Q-wave anterior wall acute myocardial infarction

The prognostic significance of angina pectoris before the development of first Q-wave anterior wall acute myocardial infarction (AMI) was assessed in 153 patients. A total of 100 patients in this study had angina before Q-wave AMI, whereas 53 patients had no antecedent symptoms of angina. The presence of angina before AMI was associated with a lower incidence of complications including sustained ventricular tachycardia or fibrillation (7% vs 25%, p = 0.0022), pump failure (24% vs 47%, p = 0.0035), cardiac rupture (1% vs 17%, p = 0.0001), and a lower inhospital mortality rate (11% vs 28%, p = 0.0067). The peak creatine phosphokinase activity was lower in patients with than without antecedent angina (1,727 ± 1,238 vs 2,675 ± 2,569 IU/liter, respectively, p = 0.023). There was no difference in the prevalence of multivessel coronary artery disease or the presence of collateral circulation between the 2 groups. Left ventriculography revealed a higher left ventricular ejection fraction (54 ± 13% vs 46 ± 11%, p = 0.034) and smaller left ventricular end-diastolic volumes (75 ± 15 vs 86 ± 18 ml/m 2, p = 0.017) in patients with than without antecedent angina. These findings suggest that the presence of angina before AMI may be associated with a protective effect on left ventricular function during anterior wall AMI. Although the precise mechanisms underlying the beneficial effects are unknown, they may be related to the development of collateral channels or ischemic preconditioning.