Absence Of Myocardial Infarction Research Articles

857 Advanced heart failure among patients with coronary artery disease in absence of myocardial infarction: prevalence, risk factors and prognosis

857 Advanced heart failure among patients with coronary artery disease in absence of myocardial infarction: prevalence, risk factors and prognosis

Lifetime risk for developing congestive heart failure: the Framingham Heart Study.

Congestive heart failure (CHF) is an increasing public health problem. Among Framingham Heart Study subjects who were free of CHF at baseline, we determined the lifetime risk for developing overt CHF at selected index ages. We followed 3757 men and 4472 women from 1971 to 1996 for 124 262 person-years; 583 subjects developed CHF and 2002 died without prior CHF. At age 40 years, the lifetime risk for CHF was 21.0% (95% CI 18.7% to 23.2%) for men and 20.3% (95% CI 18.2% to 22.5%) for women. Remaining lifetime risk did not change with advancing index age because of rapidly increasing CHF incidence rates. At age 80 years, the lifetime risk was 20.2% (95% CI 16.1% to 24.2%) for men and 19.3% (95% CI 16.5% to 22.2%) for women. Lifetime risk for CHF doubled for subjects with blood pressure >/=160/100 versus <140/90 mm Hg. In a secondary analysis, we only considered those who developed CHF without an antecedent myocardial infarction; at age 40 years, the lifetime risk for CHF was 11.4% (95% CI 9.6% to 13.2%) for men and 15.4% (95% CI 13.5% to 17.3%) for women. When established clinical criteria are used to define overt CHF, the lifetime risk for CHF is 1 in 5 for both men and women. For CHF occurring in the absence of myocardial infarction, the lifetime risk is 1 in 9 for men and 1 in 6 for women, which highlights the risk of CHF that is largely attributable to hypertension. These results should assist in predicting the population burden of CHF and placing greater emphasis on prevention of CHF through hypertension control and prevention of myocardial infarction.

Significance of anterior Q waves in left anterior fascicular block--a clinical and noninvasive assessment.

Electrocardiographic (ECG) Q waves in V leads (V2 or V3) pose a diagnostic challenge in the presence of left anterior fascicular block (LAFB). Benign Q waves in the absence of coronary artery disease (CAD) primarily due to LAFB have been described. This study evaluates Q waves in the presence of LAFB. Anterior Q waves in the presence of LAFB may not be indicative of myocardial infarction (MI). From 1990 to 1997, ECGs of 236 male patients with LAFB were analyzes for presence of Q waves in the V leads. Records were reviewed for evidence of CAD. Of 236 patients with LAFB, 61 (26%) had Q waves in the V leads. In this group, 31 patients were available for further analysis. Of the 31 patients with Q waves in the V leads who were available for further study, LAFB was present in 22 patients (71%) and LAFB plus right bundle-branch block (RBBB) were present in 9 (29%). Of 20 patients with Q waves due to MI, 13 (65%) had LAFB and 7 (35%) had LAFB plus RBBB. Of 11 patients with benign Q waves, 9 (82%) and 2 (18%) had LAFB and LAFB plus RBBB, respectively. Benign Q waves were noted in 5.3% (11/206) patients with LAFB. The mean duration of Q waves and Q-wave location limited to V2 and/or V3 are 0.029 s and 64% versus 0.053 s and 15% in benign versus pathologic Q waves, respectively. Patients with LAFB in the absence of MI may have Q waves in the V leads that are approximately 0.02 s in duration and restricted to one or two leads. This anomaly may represent a variation of conduction in the initial 0.02 s QRS vector due to LAFB.

Myocardial perfusion in patients with total occlusion of a single coronary artery with and without collateral circulation

Background. Previous studies that investigated the effects of coronary collateral circulation on myocardial perfusion were compromised by inclusion of patients with multivessel coronary artery disease, incomplete occlusion, prior myocardial infarction, or a combination of these. In this study we ascertained the relationship between angiographic collateral circulation and myocardial perfusion only in patients with total occlusion of a single coronary artery, in the absence of myocardial infarction or significant stenosis in the other coronary arteries. Methods and Results. Seventy-one consecutive patients underwent stress myocardial single photon emission computed tomography within 90 days of angiography. Collateral circulation was present in 49 patients and absent in 22 patients. All but 2 patients had abnormal perfusion by single photon emission computed tomography imaging, with a mean defect size of 19% ± 12%, and most (83%) had reversible perfusion defects. Defect count activities improved from stress to rest (or redistribution) (45% ± 13% to 59% ± 14%, P < .001). Abnormal myocardial perfusion occurred with similar frequency in patients with collateral circulation and in those without it. Total defect size was 19% ± 12% in patients with and 18% ± 11% in those without collateral circulation (P = not significant). The extent of reversibility and defect count activity during stress and rest were similar in patients with collateral circulation and in those without it. Conclusions. In patients with a single-vessel total coronary occlusion and without myocardial infarction, stress-induced myocardial ischemia is almost always present, irrespective of presence or absence of angiographic collaterals. These data lend support to the premise that collateral circulation is rather insufficient to prevent stress-induced ischemia, although it can preserve myocardial viability. (J Nucl Cardiol 2001;8:452-7.)

Evaluation of Percutaneous Laser Myocardial Revascularization in Chinese Patients with Refractory Angina Pectoris

The study aims to evaluate the feasibility and effect of percutaneous laser myocardial revascularization (PMR) in patients with refractory class III-IV angina. Patients were selected by: (1) angina class ≥III; (2) unsuitable to CABG and PTCA; (3) LVEF ≥30%; (4) absence of myocardial infarction in 6 months; (5) maximum diastolic wall thickness of left ventricle (LV) ≥8 mm in echocardiography. Eclipse Holmium laser generator and catheter were used. Eighteen patients (17 male and 1 female) with age of 63.3±7.5 years and a history of angina for 9.6±7.0 years were studied. They were refractory to 5.8±0.7 antianginal drugs. The angina class was IV in 11 patients and III in 9 patients. Maximum diastolic LV wall thickness was 10.2±0.8 mm. LVEF was 41.2±6.2%. Eleven and 9 patients had triple vessel and double vessel diffuse disease, respectively. A mean of 19.7±6.3 endomyocardial channels were made. Procedure time was 78.2±12.5 minutes and radiation time 24.3±7.4 minutes. There were no complications. During the follow-up of 18.7±1.6 months, angina class decreased from 3.8±0.7 to 2.1±0.8 (P<0.05). Ischemia in SPECT was significantly improved. PMR using Eclipse Holmium laser generator and catheter is safe in Chinese patients. This results suggest that patients with refractory class III or IV angina could be controlled by conjunctive use of PMR and regular antiangina drugs.

Long-term outcome in triple-vessel coronary artery disease in medically treated Japanese patients.

The long-term outcome in 198 patients with triple-vessel disease (TVD) treated medically was investigated. The patients, who underwent coronary angiography between September 1973 and February 1984, had significant (75% or more) stenotic lesions in all three major coronary arteries. The mean follow-up period was 8.4 years. The 5- and 10-year survival rates were 80.7% and 64.2%, respectively. Cardiac death occurred in 73 patients (36.9%) and nonfatal cardiac events developed in 60 patients (30.9%) during follow-up. When cardiac death and nonfatal myocardial infarction (MI) were defined as cardiac events, the annual attrition rate was 4.7%. There was no difference in survival with regard to the presence or absence of MI, the site of infarction, or the presence of total occlusion. In the AP group, however, the survival rate decreased as the number of totally-occluded arteries increased. In the MI group, the survival rate was not altered by the number of totally-occluded arteries, but was affected by the ejection fraction (EF). The 5-year survival rate was better in patients with good left ventricular function (EF > or = 60%) than in those with impaired left ventricular function (EF < 60%), although the 10-year survival rate was similarly low in both groups. Revascularization such as PTCA or CABG might improve the long-term outcome in patients with TVD.

Determinants of left ventricular diastolic function during myocardial ischemia: influence of myocardial structure and pericardial constraint.

To assess the influence of myocardial structure and pericardial constraint during exercise ischemia on regional left ventricular passive elastic properties. Left ventricular regional function was assessed at rest and during exercise using biplane angiography and high-fidelity pressure measurements. Twenty patients with either normal (n = 7) or stenotic coronary arteries (n = 13) were studied before and after successful bypass surgery. At the time of surgery, left ventricular transmural biopsies were taken from a normally perfused and a hypoperfused left ventricular region. Regional stiffness increased in the ischemic zone during exercise, but remained unchanged after revascularization. Regional fibrosis was significantly enhanced in the ischemic region compared with that in the normally perfused zone. No correlation was found between structural data and regional passive elastic properties, but there was a significant correlation between right atrial pressure and the asymptote of the diastolic pressure--volume relationship. Acute regional diastolic dysfunction can be observed during exercise in patients with coronary artery disease. Structural changes seem to have a minor role in the occurrence of diastolic dysfunction in the absence of myocardial infarction. The observed upward shift of the pressure-volume relationship during ischemia can be attributed to pericardial constraint that is manifested by an increase in right arterial pressure.

Cocaine-induced wide complex dysrhythmia

Cocaine is a local anesthetic with the potential to induce dysrhythmia due to direct myocardial sodium channel antagonism similar to class I antidysrhythmic drugs. The hallmark of myocardial sodium channel poisoning is wide complex dysrhythmia, and the current accepted treatment is intravenous bicarbonate. Wide complex dysrhythmia due to cocaine in the absence of myocardial infarction is rare, and optimum management is undefined. We report three cases of acute cocaine intoxication during which patients developed wide complex dysrhythmia consistent with sodium channel poisoning. In one case, wide complex tachycardia resolved without direct treatment. In the other cases, wide complex dysrhythmia resolved following intravenous bicarbonate therapy directed at reversing sodium channel blockade.

Effect of coronary angioplasty on precordial QT dispersion

Dispersion of the QT interval is a measure of inhomogeneity of ventricular repolarization. Because ischemia is associated with regional abnormalities of conduction and repolarization, we hypothesized that the surface electrocardiographic interval dispersion would increase in patients with symptomatic coronary artery disease in the absence of myocardial infarction and that successful revascularization would reduce QT interval dispersion. Thirty-seven consecutive patients with ischemia due to 1-vessel coronary artery disease without prior myocardial infarction who underwent percutaneous transluminal coronary angioplasty (PTCA) were evaluated. Standard 12-lead electrocardiograms were performed 24 hours before, 24 hours after, and late (>2 months) after PTCA. Precordial QT interval dispersions were determined from differences in the maximum and minimum corrected QT intervals. Mean QT interval dispersion before PTCA was 60 ± 9 ms, immediately after PTCA 23 ± 14 ms (p < 0.001), and late after PTCA 29 ± 18 ms (p < 0.001 vs before PTCA). The shortest precordial QT interval increased immediately after PTCA (367 ± 40 vs 391 ± 39 ms; p < 0.02) and then remained stable late after PTCA (376 ± 36 ms, p = NS vs immedately after PTCA). Symptomatic recurrent ischemia in 8 patients with documented restenosis increased QT interval dispersion (56 ± 15 ms [p < 0.01] vs 25 ± 14 ms immediately after PTCA), which decreased again after successful repeat PTCA (22 ± 13 ms [p < 0.01] vs before the second PTCA). QT interval dispersion decreases after successful coronary artery revascularization and increases with restenosis. Therefore, QT interval dispersion may be a marker of recurrent ischemia due to restenosis after PTCA.

Effect of Antithrombotic Therapy on Risk of Sudden Coronary Death in Patients With Congestive Heart Failure

Data from epidemiologic, autopsy, Holter monitoring, and electrophysiologic studies support the hypothesis that acute myocardial ischemia, even in the absence of myocardial infarction, is a critical component of the pathophysiology of sudden coronary death. Acute myocardial ischemia superimposed upon ventricles damaged from previous infarctions has been demonstrated to enhance the generation of lethal ventricular arrhythmias. This is a retrospective analysis of 6,797 participants in the Studies of Left Ventricular Dysfunction prevention and treatment trials. Both univariate and multivariate Cox proportional-hazards modeling were used to study the association of anticoagulant and antiplatelet therapy with the risk for sudden cardiac death. The following covariates were adjusted for in the analysis: age, ejection fraction, gender, atrial fibrillation, diabetes, a history of angina, prior infarction, prior revascularization, and the regular use of beta blockers, diuretics, digoxin, antiarrhythmic agents, or enalapril. The overall incidence of sudden cardiac death per 100 patient-years of follow-up was 2.24%. In multivariate analysis, antiplatelet and anticoagulant monotherapy each remained independently associated with a reduction in the risk of sudden cardiac death: antiplatelet therapy with a 24% reduction (relative risk [RR] 0.76; 95% confidence interval [CI] 0.61–0.95) and antiplatelet monotherapy with a 32% reduction (RR 0.68; 95% CI 0.48–0.96). Thus, in patients with moderate to severe left ventricular systolic dysfunction resulting from coronary artery disease, antiplatelet and anticoagulant therapy are each associated with a reduction in the risk of sudden cardiac death.This is a retrospective database analysis of the Studies of Left Ventricular Dysfunction (SOLVD) prevention and treatment trials. We examined the association of antiplatelet and anticoagulant therapy with the risk for sudden cardiac death. In both univariate and multivariate analyses, both antiplatelet and anticoagulant therapy were each associated with a significant reduction in the risk for sudden cardiac death.

Long-term outcome in double-vessel coronary artery disease in Japanese patients.

The long-term (average: 10 years) outcome in 220 patients with double-vessel disease (DVD) treated medically was investigated. The patients underwent coronary angiography between September 1973 and February 1984, and significant (75% or more) stenosis was detected in each of two major coronary arteries. These patients showed relatively good 5-year and 10-year survival rates of 94.5% and 87.4%, respectively. Cardiac death occurred in 31 patients (14.1%) and nonfatal myocardial infarction (MI) developed in 16 patients (7.3%) during follow-up. When these were defined as cardiac events, the annual attrition rate was 3.1%. A comparison of the outcome with regard to the presence or absence of MI revealed worse results for the MI group, but no difference was observed between different sites of infarction. There was also no difference in outcome with regard to the presence or absence of lesions in the left anterior descending artery (LAD). In the MI group, patients with impaired left ventricular function (ejection fraction < or = 40%) had inferior survival to those with good left ventricular function. Thus, DVD associated with good left ventricular function had a relatively good outcome when treated medically, while patients with impaired left ventricular function might benefit from revascularization.

Hibernating myocardium, a clinical entity

Before the term “hibernating myocardium” was introduced by Rahimtoola (1), it was shown by us that a subpopulation of patients could be defined who had a significant coronary artery stenosis and impaired wall motion in the absence of myocardial infarction (2). These patients could only be identified by a multivariate analysis using parameters related to preoperative regional wall motion, electrocardiogram, severity of coronary stenosis and viability of the myocardium. Data on myocardial viability were derived from histological examination of intraoperatively obtained biopsy material.

Identification of myocardial reperfusion with echo planar magnetic resonance imaging. Discrimination between occlusive and reperfused infarctions.

The current treatment of many cases of acute myocardial infarction involves the use of thrombolytic agents. Evaluation of this therapy requires determination of the success of reperfusion and assessment of the presence and extent of infarction in the reperfused territory. The present study was designed to simulate in rat models several possible outcomes of reperfusion therapy: (1) successful reperfusion and absence of myocardial infarction, (2) successful reperfusion and presence of myocardial infarction, and (3) unsuccessful reperfusion. The usefulness of contrast-enhanced fast magnetic resonance (MR) imaging in defining the success of reperfusion was investigated. The dynamic effects were examined of low and high doses of gadolinium-BOPTA/dimeglumine (Gd-BOPTA/dimeg) on myocardial signal using MR inversion recovery echo planar imaging (IR-EPI) and gradient recalled echo planar imaging (GR-EPI), respectively. Rats were subjected to one of the following regimens: reperfused reversible myocardial injury (n = 9), reperfused irreversible myocardial injury (n = 9), and occlusive infarction (n = 9). MR echo planar images were acquired every 1 or 2 seconds before, during, and after administration of Gd-BOPTA/dimeg. In all groups, normal myocardial signal was sharply increased on IR-EPI and decreased on GR-EPI at the peak of the bolus, followed by a gradual decline to baseline. In animals subjected to reperfused reversible myocardial injury, normal and previously ischemic regions were indistinguishable during and after the passage of Gd-BOPTA/dimeg. On the other hand, enhancement of reperfused irreversibly injured myocardium was delayed but increased steadily to a higher level than normal myocardium on IR-EPI. The reperfused irreversibly injured myocardium was identified on IR-EPI as a zone of high signal (hot spot). On GR-EPI, signal loss in reperfused irreversibly injured myocardium was significantly less compared with normally perfused myocardium. In animals with occlusive infarctions, there was no change in signal intensity over the ischemic region on either IR-EPI or GR-EPI. Occlusive infarction was identified as zones of either low (cold spot) or high (hot spot) signal compared with normal myocardium, depending on MR pulse sequence and dose of the contrast medium. The transit of Gd-BOPTA/dimeg monitored by fast MR imaging techniques can be used to distinguish between reperfused reversibly and reperfused irreversibly injured myocardium and between occlusive and reperfused infarctions.

Pathobiology of sudden death: coronary causes

The single most common cause of sudden death in the western world is coronary artery disease. Sudden death from coronary causes occurs equally in asymptomatic patients, patients with angina, and patients with a known history of myocardial infarction. The mechanism of sudden coronary death in most patients is ventricular fibrillation secondary to ischemia. Microthrombi in intramyocardial coronary arteries may also play a role. Instability of atherosclerotic plaques, in terms of thrombosis and vasoreactivity, underlies the syndrome of unstable angina as well as many cases of acute myocardial infarction. Sudden coronary death falls within this spectrum of ischemic heart disease. Development of these syndromes depends on the abruptness of onset and the completeness and duration of coronary occlusion. Thus a rapidly evolving coronary artery lesion, with plaque fissure, rupture, and luminal thrombosis, can lead to myocardial ischemia, with fatal electrical instability of the myocardium as the first clinical manifestation. The diagnosis of sudden coronary death in the absence of myocardial infarction is determined by the degree of coronary artery narrowing and the exclusion of other causes of death. The presence of acute coronary artery lesions, which may be present in a significant number of sudden coronary death patients, lends support to the pathologic diagnosis. Thus the coronary arteries in victims of sudden coronary death may exhibit established atherosclerotis or acute lesions, whereas the myocardium may appear normal or show healed or acute infarction or hypertrophy. Although less common, nonatherosclerotic coronary artery diseases can account for sudden death as well, particularly in younger patients. Therefore, when sudden death occurs in children and young adults, coronary causes related to congenital anomalies, fibromuscular dysplasia, arteritis, or metabolic diseases should be considered.

Changes in septal regional ejection fraction early and late following coronary artery bypass grafting in patients without postoperative myocardial infarction

Changes in regional ejection fraction (rEF) of the interventricular septum following coronary artery bypass graft (CABG) surgery were examined using first-pass radionuclide ventriculography (RNVG) in patients without objective evidence of postoperative myocardial infarction (MI). One hundred and one patients had pre- (mean 6.3 days) and early postoperative (mean 8.7 days) RNVGs, and 60 of these patients had follow-up studies at 14-39 months (mean 27 months) postsurgery. Early post-CABG, mean rEF in the proximal septum was unchanged from the preoperative value (35.3%), with almost equal numbers of patients showing increased (n = 36), unchanged (n = 33) or decreased (n = 32) rEFs. In the distal septum, mean rEF increased from 47.1 to 50.7%, with more than twice as many patients having increased (n = 44) as decreased (n = 20) rEF. At late follow-up, proximal septum rEF in individual patients tended to revert to the presurgery baseline, with 72% (13/18) of regions with early decrease improved and 61% (14/23) of those with early improvement decreased. In the distal septum, rEF was less than early post-CABG in 76% (19/25) of patients with early improvement, while being improved in 27% (3/11) of those with early decrease in rEF. In the absence of MI, changes in rEF in the proximal septum early post-CABG tend to resolve over time. While global changes in cardiac systolic motion are the probable cause of many new post-CABG septal abnormalities, persistent septal dysfunction probably reflects effects of permanent damage as a result of the operative procedure.

Changes in septal regional ejection fraction early and late following coronary artery bypass grafting in patients without postoperative myocardial infarction

Summary Changes in regional ejection fraction (rEF) of the interventricular septum following coronary artery bypass graft (CABG) surgery were examined using first-pass radionuclide ventriculography (RNVG) in patients without objective evidence of postoperative myocardial infarction (MI). One hundred and one patients had pre- (mean 6.3 days) and early postoperative (mean 8.7 days) RNVGs, and 60 of these patients had follow-up studies at 14-39 months (mean 27 months) postsurgery. Early post-CABG, mean rEF in the proximal septum was unchanged from the preoperative value (35.3%), with almost equal numbers of patients showing increased (n = 36), unchanged (n = 33) or decreased (n = 32) rEFs. In the distal septum, mean rEF increased from 47.1 to 50.7%, with more than twice as many patients having increased (n = 44) as decreased (n = 20) rEF. At late follow-up, proximal septum rEF in individual patients tended to revert to the presurgery baseline, with 72% (13/18) of regions with early decrease improved and 61% (14/23) of those with early improvement decreased. In the distal septum, rEF was less than early post-CABG in 76% (19/25) of patients with early improvement, while being improved in 27% (3/11) of those with early decrease in rEF. In the absence of MI, changes in rEF in the proximal septum early post-CABG tend to resolve over time. While global changes in cardiac systolic motion are the probable cause of many new post-CABG septal abnormalities, persistent septal dysfunction probably reflects effects of permanent damage as a result of the operative procedure.

Effect of maximal medical therapy on refractoriness of unstable angina pectoris

A group of 125 patients with unstable angina were studied over a 5-year period to define the incidence of refractory unstable angina in the current era of 5-drug medical therapy with intravenous heparin, aspirin, nitrates, calcium antagonists andβ blockers. All patients had >20 minutes of chest pain at rest with reversible electrocardiographic changes occurring in the absence of myocardial infarction. Patients were considered refractory only if chest pain continued despite treatment with maximal 5-drug therapy. At the time of transfer to the center, 65 patients continued to have ischemic chest pain at rest and were considered “medically refractory” by their referring physicians. A more aggressive medical regimen was used, and 54 patients (83%) were rendered chest pain-free. Of the 11 truly refractory patients (8.8%), coronary arteriography revealed an increased likelihood of left main or 3-vessel disease (7 of 11 vs 26 of 114; p = 0.01). Inhospital treatment strategies for the 114 patients stabilized with medical therapy included continued medical therapy (n = 37), coronary angioplasty (n = 46) and bypass grafting (n = 31). The rate of myocardial infarction or death in patients managed medically was 3%. Coronary angioplasty in medically stabilized patients was complicated by an abrupt closure rate of 26%, and a 17% rate of myocardial infarction, death or need for emergency bypass grafting. Medically stabilized patients undergoing bypass grafting had a 9% rate of myocardial infarction or death. Unstable angina truly refractory to current, maximal medical therapy is infrequent (8.8%). However, the refractory group is vulnerable to adverse angioplasty results and cardiac events.

Coronary angioplasty with second generation Monorail catheters

The Monorail system (Schneider) consists of a balloon catheter in which the guidewire passes through the balloon itself, exits the catheter proximal to the balloon, and runs alongside its small shaft (3 French) through the length of the guiding catheter. It offers distinct advantages over conventional systems of coronary angioplasty. It facilitates contrast injections and permits rapid balloon exchanges. This system was used for coronary angioplasty in 273 unselected consecutive patients (age 59 ± 10, mean 35 to 73 years). There were 216 patients (84%) undergoing single-vessel and 57 patients (16%) with multi-vessel coronary angioplasty. A total of 335 coronary stenoses were dilated, which included 35 total occlusions. The size of balloon used ranged from 2.0 to 4.25 mm (3.0 ± 0.5 mm) and the severity of stenosis was 85 ± 11%. Technical success was defined as a residual stenosis of less than 50% as determined angiographically. Clinical success was defined as technical success, and absence of a major inhospital complication defined as absence of myocardial infarction, lack of need for coronary arterial bypass surgery, and survival. The Monorail system was technically successful in 294 300 stenotic lesions (98%). It was clinically successful for 281 lesions (94%). Of the 35 total occlusions, technical success was obtained in 25 (71%). The residual stenosis of successful cases was 26 ± 21%. The Monorail system was also successful in 5 patients with stenosis of more than 90% in whom conventional systems failed. The complications included acute occlusion causing acute myocardial infarction in 13 cases (5%), emergency coronary arterial bypass surgery in 1 patient (0.4%), and death in 4 patients (1.5%). These results indicate that the second generation Monorail catheters can be used effectively for angioplasty of coronary stenoses and total coronary occlusions.

Reduction of myocardial infarction after emergency coronary artery bypass grafting for failed coronary angioplasty with use of a normothermic reperfusion cardioplegia protocol

Emergency coronary artery bypass grafting is necessary in 2.7% to 13.5% of patients undergoing elective percutaneous transluminal coronary angioplasty. Myocardial infarction develops in 11% to 49% of these patients, with 18% to 46% of infarcts resulting in new Q waves. Since February 1987 a revised protocol for myocardial preservation has been used in 19 patients undergoing emergency bypass grafting for failed angioplasty. Cardioplegia is induced with a normothermic blood cardioplegic solution. Multiple maintenance doses of cold (4 degrees C) blood cardioplegic solution are then delivered through the aortic root and vein grafts. Before the aortic crossclamp is removed, normothermic reperfusion cardioplegic solution is delivered through the aortic root and vein grafts. This group was compared with all patients undergoing emergency bypass grafting for failed angioplasty before February 1987. These 45 patients received cold induction of cardioplegic solution, multiple maintenance doses of cold cardioplegic solution, and no reperfusion cardioplegic solution. The prevalence of myocardial infarction in the group receiving cold cardioplegic solution was 65% versus 26% in the group receiving normothermic cardioplegic solution (p less than 0.007). Multivariate analysis identified the use of the normothermic cardioplegia protocol (p less than 0.005), nontotal occlusion of the angioplasty vessel (p less than 0.03), and presence of collateral flow to the angioplasty vessel (p less than 0.04) as being independently associated with absence of myocardial infarction.

The relationship between chest pain during Thallium-201 scintigraphy with dipyridamole and myocardial ischemia.

Dipyridamole thallium-201 scintigraphy (DP-Tl) and coronary angiography were studied on 74 patients with suspected coronary artery disease. We compared the clinical features, hemodynamic responses, angiographic results and scintigraphic findings of patients who had chest pain during DP-Tl testing ('chest pain' group) with those of patients who did not have chest pain ('no pain' group). Thirty eight (51%) of the 74 patients developed chest pain. Heart rate and rate pressure product during DP infusion of 'chest pain' group were greater than those of the 'no pain' group (p less than 0.05). Ischemic ST depression was more frequently observed among 'chest pain' patients (p less than 0.01). There were no differences in angiographic severity of coronary artery disease between 'chest pain' and 'no pain' group. Also, we could find no differences in extent and severity scores of perfusion defects and washout abnormalities between the two groups. However, when patients with myocardial infarction were excluded, the 'chest pain' group had significantly greater extent and severity scores of washout abnormalities than the 'no pain' group (extent score: 38 +/- 8 vs 18 +/- 5, p less than 0.05, severity score: 55 +/- 15 vs 18 +/- 7, p less than 0.01). Our study indicated that in patients without myocardial infarction, patients with 'chest pain' had more severe ischemia than 'no pain' patients. But in patients with myocardial infarction, myocardial ischemia not accompanied by chest pain might be as severe as that with chest pain. The presence or absence of myocardial infarction might have great influence on results regarding the relation of chest pain to myocardial ischemia.