Long-term follow-up after direct percutaneous transluminal coronary angioplasty for acute myocardial infarction.

OBJECTIVES: The purpose of this study was to analyze long-term follow-up information over several years from consecutive, unselected patients treated with direct percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (MI). BACKGROUND: Direct PTCA is often used in patients with acute MI. Short-term results are favorable. However, there is less information available on long-term observations over several years in these patients. METHODS: A total of 416 consecutive and unselected patients with acute MI underwent direct PTCA. Survival of the acute infarct phase was 94.2%; the remaining 392 patients--the study population-were discharged and followed for 3.3+/-1.4 years. Mortality as well as cardiac events and reinterventions are reported. Clinical variables assessed at the time of discharge are submitted to statistical analysis to detect potential risk factors. RESULTS: Total cumulative mortality in the first year was 10% for the entire group and 6% for patients not presenting in cardiogenic shock. Mortality after discharge was 4.6% in the first year and dropped to <4% per year thereafter. Reinterventions after discharge were required in 16% in the first year and in <4% per year in years 2 to 4. Poor left ventricular ejection fraction (<35%), three-vessel disease and advanced age (> or =75 years) were long-term risk factors for total mortality after direct PTCA. CONCLUSIONS: The clinical benefit of direct PTCA for acute MI is maintained during follow-up with respect to mortality. However, reinterventions for restenosis or de novo stenosis are often required (10% to 20%). Although few in number (<10%), patients with severely impaired left ventricular function continue to have a poor prognosis.

Type 2 diabetes and acute myocardial infarction. Angiographic findings and results of an invasive therapeutic approach in type 2 diabetic versus nondiabetic patients.

OBJECTIVE: Mortality in diabetic patients with acute myocardial infarction (MI) is high. The significance of the pretreatment coronary status in type 2 diabetic patients with acute MI, as well as the effect of mechanical revascularization using percutaneous transluminal coronary angioplasty (PTCA), has not been established. RESEARCH DESIGN AND METHODS: All patients with type 2 diabetes and acute MI (n = 54) were prospectively enrolled into a study of immediate coronary angiography to guide PTCA of the occluded infarct vessel. Hospital and long-term course were assessed and compared with an unselected control group of nondiabetic patients (n = 358) who were enrolled in the same study. RESULTS: Angiography showed that sites of occlusion and acute coronary flow were similar in both groups. Multivessel disease and shock were more common in type 2 diabetic versus nondiabetic patients: 69 vs. 51% and 21 vs. 10% (P < 0.02), respectively. Direct PTCA was successful in > 90% in both groups. Mortality after 30 days was 13% in type 2 diabetic patients versus 5% in patients without diabetes (P < 0.04). Left ventricular (LV) ejection fraction before discharge was lower in diabetic patients (48 +/- 17 vs. 55 +/- 15%, P < 0.05). Mortality 1 year after discharge was 11 vs. 4% in diabetic versus nondiabetic patients (P < 0.02). Multivariate analysis identified type 2 diabetes as an independent risk factor for acute, but not for late, mortality. CONCLUSIONS: Direct PTCA is safe and effective in type 2 diabetic patients with acute MI. Mortality after 30 days in unselected diabetic patients is < 15% with this approach. Advanced disease and shock contribute to an increased mortality in type 2 diabetic patients with acute MI versus nondiabetic patients.

The expression of angiotensin-I converting enzyme in human atherosclerotic plaques is not related to the deletion/insertion polymorphism but to the risk of restenosis after coronary interventions.

Plasma and tissue concentrations of the angiotensin-I converting enzyme (ACE) have been shown to be associated with the ACE insertion/deletion (I/D) polymorphism. The purpose of this study was to examine the relation of ACE levels in atherosclerotic plaques to the ACE I/D polymorphism and to restenosis after balloon angioplasty and directional atherectomy (DCA). The study included 104 patients who underwent DCA and received angiographic follow-up at 12 to 18 months. The amount of ACE protein in various morphologically defined plaque components (fibrous, atheromatous, and complicated lesions) of the atherectomy specimens was determined by qualitative and semiquantitative immunohistochemistry. ACE levels were related to the ACE genotype, to plaque morphology and to the risk of restenosis. Sequential staining revealed that pathologic ACE overexpression of the atherosclerotic lesions occurred in intimal smooth muscle cells, fibrocytes/fibroblasts and macrophage/foam cells. The ACE content of the whole plaques and of the single plaque components was not associated with the I/D polymorphism, but with restenosis after coronary interventions. In addition, ACE levels in the atherosclerotic lesions correlated with the severity of vessel wall damage. The ACE phenotype might serve as an indicator for the risk of restenosis after coronary interventions.

Positive association of the beta fibrinogen H1/H2 gene variation to basal fibrinogen levels and to the increase in fibrinogen concentration during acute phase reaction but not to coronary artery disease and myocardial infarction.

BACKGROUND: Fibrinogen has been demonstrated to be an independent risk factor of cardiovascular disease. The absence of the HaeIII cutting site (H2 allele) of an H1/H2 gene variation in the promoter region of the beta fibrinogen gene was associated with increased levels of fibrinogen. METHODS AND RESULTS: In the present study, the effects of the H1/H2 gene variation not only on plasma fibrinogen concentrations but also on coronary artery disease (CAD) and myocardial infarction (MI) were investigated in 923 individuals who underwent coronary angiography for diagnostic purposes. Relation of the H1/H2 genotype to fibrinogen plasma levels: A strong association was observed between the H1/H2 gene variation and fibrinogen levels. The differences in fibrinogen plasma levels between H2H2 and H1H1 homozygotes were almost threefold more pronounced within subjects with clinical chemical signs of an acute phase reaction (CRP > or = 7.5 mg/l) than within a subgroup of subjects without these signs (CRP < 7.5 mg/l) (median of CRP distribution: 7.5 mg/l). In 207 patients who underwent aortocoronary bypass surgery plasma fibrinogen levels were almost identical directly after surgery. Two days after operation fibrinogen increased to clearly higher levels in H2H2 homozygotes than in H1H2 and H1H1 genotypes, whereas almost the same maximal increases in fibrinogen concentrations were reached 3-4 days after surgery in all individuals. Relation of the H1/H2 genotype to CAD and MI. Whereas in the total population the plasma fibrinogen concentrations were strongly associated with smoking, CAD and MI, an association of the H1/H2 gene variation to CAD and MI was not detected. However, mean age at first MI of H2H2 individuals (62.9 years) was clearly higher than of H1H2 genotypes (56.9 years) and of H1H1 subjects (56.4 years). In addition, in a subgroup of individuals with a higher risk of MI by either high apoB and/or low apoA1 plasma levels the portion of MI patients was clearly smaller within H2H2 homozygotes than within H1H2 or H1H1 genotypes, although-also in these high risk groups-mean age at first MI of H2H2 individuals were higher than of the other two genotypes. CONCLUSIONS: Obviously, the H2 allele of the fibrinogen H1/H2 genotype does not only influence basal fibrinogen concentrations, but particularly also the extent of fibrinogen level increase during acute phase reaction. Whereas the fibrinogen plasma level is positively associated with coronary artery disease and myocardial infarction, the H2 allele-although exhibiting an association with elevated fibrinogen levels-was not positively associated with CAD and MI.

Results and significance of Holter monitoring after direct percutaneous transluminal coronary angioplasty for acute myocardial infarction.

Whether acute and direct percutaneous transluminal coronary angioplasty improves the incidence of nonsustained ventricular tachycardia in patients surviving acute myocardial infarction is not known. In 400 consecutively studied patients, Lown classification IVb on Holter monitoring was only associated with arrhythmia morbidity, whereas reduced ejection fraction was related to total and cardiac mortality and arrhythmia morbidity.

Calcium antagonists and myocardial microperfusion.

Recent studies have improved our understanding of the beneficial actions of calcium antagonists on myocardial microcirculation and metabolism. The effect of calcium antagonists on the microcirculation of the left ventricular rat myocardium was studied using in vivo microscopic techniques. Intravenous verapamil 0.3 mg/kg and nifedipine 75 micrograms/kg produced a 15 to 18% increase in the diameter of larger A1 and A2 coronary arterioles (range 31 to 300 microns); diameters of terminal (A4) arterioles and capillaries did not change significantly. Furthermore, verapamil significantly (p less than 0.001) increased the ratio of capillaries filled with red cells to those containing plasma alone. Verapamil pretreatment produced a similarly selective dilatation of larger coronary arterioles and protected against the ischaemia-induced fall in capillary red cell content. Spectroscopic data show that verapamil also produces an increase in myocardial phosphocreatine and preservation of adenosine triphosphate (ATP) during ischaemia in the Langendorff-perfused heart. In patients with exercise-induced angina, gallopamil decreased global myocardial 201Tl and 123I phenylpentadecanoic acid (IPPA) uptake due to a reduction in myocardial oxygen consumption. Regional 201Tl and IPPA uptake as well as IPPA clearance in post-stenotic areas tended to rise after gallopamil treatment. Thus, the beneficial effects of calcium antagonists such as verapamil or gallopamil in patients with ischaemic heart disease may result from dilatation of predominantly larger arterioles. Consequently, there is an improvement in regional perfusion and free fatty acid utilisation in reversibly ischaemic regions.

[Haemophilus aphrophilus as the causative agent in a case of bacterial sepsis]. / Haemophilus aphrophilus als Erreger einer bakteriellen Sepsis.

Haemophilus aphrophilus was isolated from 5 blood cultures of a 31-year-old male patient who developed septicaemia two years after heart surgery. The bacteriological and clinical properties of H. aphrophilus are discussed in view of the available literature.

Purification of a model substrate for transcription factor phosphorylation by ERK2.

ERK2 belongs to the mitogen-activated protein kinase subfamily, which plays a pivotal role in cell signal transduction, in which it mediates effects on proliferation and differentiation by growth factors and hormones. While its cellular function has been under intense scrutiny since its initial discovery nearly 15 years ago, little progress has been made in understanding its kinetic mechanism. Such an understanding is important for the development of potent and specific inhibitors. A contributory factor has been the lack of a protein substrate suitable for rigorous mechanistic studies. Here we report the expression, purification, and characterization of the N-terminus (residues 1 through 138) of the transcription factor Ets-1, an excellent model substrate for ERK2 mechanistic studies. (His(6)-tagged)Ets-1(1-138) was expressed in Escherichia coli and rapidly purified in two steps by nickel-agarose-affinity chromatography, followed by high-resolution Mono-Q anion-exchange chromatography. A yield of 60 mg of the purified protein per liter of culture was obtained and could be stored conveniently at -80 degrees C in water. Rigorous characterization demonstrated that under the assay conditions, (His(6)-tagged)Ets-1(1-138) is exclusively phosphorylated on residue Thr-38 by ERK2 with the following Michaelis parameters: k(cat) = 17 s(-1), K(ATP)(m) = 140 microM, K(ATP)(i) = 68 microM, K(Ets-1)(m) = 19 microM, and K(Ets-1)(i) = 9.3 microM.

Chemiluminescent determination of adenosine, inosine, and hypoxanthine/xanthine.

A fully automatic method for analysis of adenosine, inosine, and hypoxanthine/xanthine which combines the specificity of enzymatic catalysis and sensitivity of chemiluminescence is presented. The hydrogen peroxide formed by sequential catabolism of purines to uric acid is detected by the oxidation of luminol in the presence of peroxidase. The method takes advantage of the fact that light output in the H2O2/luminol system is transient. By adopting a two-step procedure this feature enables selective determination of adenosine, inosine, and hypoxanthine/xanthine. In step 1 any purines lower in the catabolic sequence than the analyte under study are converted to uric acid. Light emission is allowed to decay to baseline levels. During step 2 the analyte is selectively degraded. The H2O2 formed leads to a new light emission which is proportional to the square of analyte concentration. The method can be performed with commercially available reagents and enzymes and requires minimal processing of biological samples. Excellent agreement has been obtained with HPLC analysis. Sensitivity is in the range of 5-10 nmol/liter in as little as 0.1 ml. More than 200 samples per day can be analyzed by a single operator.

Endolaryngeal high-frequency ultrasound.

High-frequency ultrasound can provide high-resolution imaging for diagnosing diseases of the head and neck. Over the last few years, a virtual technical evolution has led to the development of small and flexible ultrasound transducers with even greater anatomic resolution. The aim of the present study was to evaluate the efficacy of this new technique for imaging normal and altered anatomical structures of the endolarynx. Specially developed high-resolution, real-time ultrasound transducers (10 and 20 MHz) placed on the tip of endoluminal catheters were inserted into 20 autopsied larynges and five laryngectomy specimens. In a standardized examination process the endolarynx was analyzed in a real-time mode. Using this technique, exact 360 degrees cross sections of the larynx were obtained, demonstrating that it was possible to image the structures of the endolarynx with ultrasonography. Depending on the frequency used, all anatomical structures could be visualized up to a depth of 2 cm. In laryngeal cancer the depth of tumor as well as its relationship to the laryngeal framework could be clearly recognized. These findings suggest that this new endoluminal sonographic procedure represents a potentially important diagnostic tool in the assessment of laryngeal carcinoma.

The kinetic mechanism of the dual phosphorylation of the ATF2 transcription factor by p38 mitogen-activated protein (MAP) kinase alpha. Implications for signal/response profiles of MAP kinase pathways.

The mitogen-activated protein kinases (MAPKs) are a family of enzymes conserved among eukaryotes that regulate cellular activities in response to numerous external signals. They are the terminal component of a three-kinase cascade that is evolutionarily conserved and whose arrangement appears to offer considerable flexibility in encompassing the diverse biological situations for which they are employed. Although multistep protein phosphorylation within mitogen-activated protein kinase (MAPK) cascades can dramatically influence the sensitivity of signal propagation, an investigation of the mechanism of multisite phosphorylation by a MAPK has not been reported. Here we report a kinetic examination of the phosphorylation of Thr-69 and Thr-71 of the glutathione S-transferase fusion protein of the trans-activation domain of activating transcription factor-2 (GST-ATF2-(1-115)) by p38 MAPKalpha (p38alpha) as a model system for the phosphorylation of ATF2 by p38alpha. Our experiments demonstrated that GST-ATF2-(1-115) is phosphorylated in a two-step distributive mechanism, where p38alpha dissociates from GST-ATF2-(1-115) after the initial phosphorylation of either Thr-69 or Thr-71. Whereas p38alpha showed similar specificity for Thr-71 and Thr-69 in the unphosphorylated protein, it displayed a marked difference in specificity toward the mono-phosphoisomers. Phosphorylation of Thr-71 had no significant effect on the rate of Thr-69 phosphorylation, but Thr-69 phosphorylation reduced the specificity, k(cat)/K(M), of p38alpha for Thr-71 by approximately 40-fold. Computer simulation of the mechanism suggests that the activation of ATF2 by p38alpha in vivo is essentially Michaelian and provides insight into how the kinetics of a two-step distributive mechanism can be adapted to modulate effectively the sensitivity of a signal transduction pathway. This work also suggests that whereas MAPKs utilize docking interactions to bind substrates, they can be weak and transient in nature, providing just enough binding energy to promote the phosphorylation of a specific substrate.

Improvement of diastolic filling in hypertensive patients treated with cilazapril.

The aim of this study was to assess the behavior of the diastolic left ventricular (LV) filling pattern and cardiac hypertrophy after treatment with cilazapril. Twelve patients (9 male and 3 female) with mild to moderate essential hypertension, aged 46 +/- 14.1 years, were treated with cilazapril for 1 year. They underwent Doppler echocardiography at the beginning (I), after 6 months (II), and after 1 year (III) of treatment. The following parameters were evaluated: mean arterial pressure (MAP) automatically recorded for 24 h, interventricular septal and posterior wall thickness, LV and end-diastolic diameter, LV mass index, early (E) and late (A) diastolic filling flow velocities, and the ratio E/A. A significant reduction in LV hypertrophy and an improved diastolic filling pattern of the left ventricle was shown after 6 months of therapy with cilazapril; this improvement still remained after 1 year of therapy.

[Persistent angina pectoris in spite of successful myocardial revascularisation]. / Fortbestehende Angina pectoris trotz erfolgreicher Myokardrevaskularisation.

A 73-year-old obese woman underwent coronary artery-bypass operation in 11/1995 because of a coronary two vessel disease. The left coronary artery was bypassed by the left mammarial internal artery. In 2 and 3/2002, balloon-dilatation of stenoses of the right coronary artery and the circumflex was performed. Angina pectoris relapsed and in 9/2002 the patient was admitted to our hospital with tentative diagnosis of restenosis. Physical investigation showed a blood pressure of the right arm of 160/80 and of the left arm of 120/ 80 mmHg. Coronarography showed the three vessel disease known since 2/2002 with a restenosis of the right coronary artery which was immediately treated by balloon-dilatation and stent-implantation. Colour duplex-sonography of the carotid and subclavian arteries revealed extraordinary plaques and a reduced flow of the left vertebral artery. The left subclavian artery could only be seen distal to the discharge of the vertebral artery and showed a poststenotic flow. The patient had angina pectoris when carrying out personal hygiene already 2 days after balloon-dilatation and stent-implantation. ECG showed new aspects. Coronarography showed no relapse of stenosis, but 70% stenosis of the left subclavian artery with a marked coronary-steal-syndrome. In 10/ 2002, the patient underwent balloon-dilatation and stent-implantation of the subclavian stenosis and became free of complaints. Coronary-steal-syndrome can be the reason for persistent angina pectoris in spite of successful coronary artery-bypass operation with a mammarial internal bypass. It is absolutely necessary to take blood pressure from both arms to recognise a possible stenosis of the subclavian artery which can be the key to all.

Low prevalence of Chlamydia pneumoniae in atherectomy specimens from patients with coronary heart disease.

Coronary atherectomy specimens from 50 patients with coronary heart disease were examined for the presence of Chlamydia pneumoniae by two different methods of polymerase chain reaction (PCR) and by in situ hybridization. C. pneumoniae DNA was detected by PCR in atherosclerotic plaques of four patients (8%). Two patients' coronary atheromas were positive, both by a single-step 16S rRNA-based PCR and by an omp1-based nested PCR. The other two patients' specimens were positive only by the nested PCR. In contrast, C. pneumoniae was not detected by in situ hybridization in any of the cardiovascular tissues tested. Of three patients with evidence of C. pneumoniae in coronary atheromas, two had an antibody titer of 1:32 and the third had no specific antibodies detectable. Results of this study demonstrate a low prevalence of C. pneumoniae DNA in coronary atheromas. These findings do not support the hypothesis that the organism plays a major role in atherogenesis.

[Disorders of microcirculation in coronary heart disease]. / Störungen der Mikrozirkulation bei der koronaren Herzkrankheit.

Disturbances of microcirculation in coronary artery disease can be seen in the presence of critical stenosis of epicardial coronary arteries, as a result of endothelial dysfunction in the absence of significant stenosis or during recovery of ischaemic myocardium after successful angioplasty of stenosed or occluded coronary arteries. Diagnostic methods are morphologic/morphometric analyses, measurement of the global coronary reserve, measurement of the regional coronary microcirculation (scintigraphy, positron emission tomography) and laboratory analysis of haemorheological alterations (plasma, erythrocytes, leucocytes). After successful angioplasty, normalisation of glutamate extraction rate takes three to six months. In patients with unstable angina, changes in plasma viscosity, erythrocyte aggregation and neutrophil activation occur. Neutrophils are activated after successful angioplasty in acute myocardial infarction and even after elective angioplasty (when measured in the coronary sinus). Therapeutic improvements of disturbed microvascular flow can be obtained by increasing perfusion pressure (by revascularisation, nitrates, calcium antagonists, physical training), by improving the fluidity of the blood and by reducing the extravascular component of coronary vascular resistance (by antihypertensive treatment).

Improvement of cardiac function by angiotensin converting enzyme inhibition. Sites of action.

BACKGROUND: The discovery of new properties of angiotensin converting enzyme (ACE) inhibitors in addition to their well-known ability to lower blood-pressure, such as antiproliferative actions and antiadrenergic and vagal-stimulating effects, has contributed to the usefulness of this class of agents in the prevention and treatment of cardiovascular diseases. METHODS AND RESULTS: The contribution of an activated endocrine and/or cardiac paracrine renin-angiotensin system to the progression of cardiovascular diseases with the exception of renovascular hypertension is not fully understood. In particular, the following questions were addressed: 1) Is the facilitation of noradrenaline release in the genesis of arrhythmias a target for ACE inhibition? 2) Is an impaired nutritional cardiac blood flow in heart failure a target for ACE inhibition? 3) Is the intimal hyperplasia that results from coronary angioplasty a target for ACE inhibition? 4) Is the diastolic dysfunction associated with left ventricular hypertrophy in essential hypertension a target for ACE inhibition? In an isolated rat heart preparation with ischemia-induced arrhythmias, none of the ACE inhibitors nor an angiotensin II antagonist was able to significantly suppress the incidence or severity of arrhythmias. In 12 patients with New York Heart Association functional class II-IV heart failure, a fall in cardiac filing pressures after ACE inhibition was associated with an immediate rise in cardiac output and an increase in coronary blood flow of almost 30%. In 24 patients with angina at rest, a preceding percutaneous transluminal coronary angioplasty, and a second angioplasty, control angiograms at 6 months revealed a high degree of restenosis in both ACE inhibitor-treated and placebo patients. Luminal narrowing amounted to 72% in the placebo group and 61% in the ACE inhibitor group. The differences between placebo and enalapril were statistically not significant. In 12 patients with essential hypertension treated with 5 mg cilazapril, left ventricular mass was reduced by 30%, which was closely related to the change in mean arterial blood pressure. The concomitant normalization of the diastolic filling pattern by ACE inhibition, however, was not related to the respective changes in blood pressure. CONCLUSIONS: Promising experimental data regarding the antiproliferative effects of ACE inhibitors in preventing restenosis could not be transferred into clinical benefits for patients who underwent repeat coronary angioplasty. Possible antiarrhythmic effects of ACE inhibitors are not likely to be caused by their suppression of noradrenaline release during myocardial ischemia. ACE inhibition was effective in reducing coronary resistance in patients with severe heart failure, thereby augmenting nutritional cardiac blood flow. ACE inhibition also effectively induced a regression of left ventricular hypertrophy in essential hypertension. The associated normalization of diastolic filling pattern may represent an important goal in the treatment of hypertension.

[Long-term follow-up after direct PTCA in women with acute myocardial infarction]. / Langzeitbefunde der primären Angioplastie bei Frauen mit akutem Myokardinfarkt.

METHODS: Long-term follow-up of 204 consecutive and unselected women vs 577 men after direct PTCA for acute myocardial infarction. RESULTS: Women were older, had more significant comorbidity, and had a longer prehospital phase. Direct PTCA of the infarct artery was angiographically successful in 95% of women and in 94% of men. Total cumulative mortality during 4 years of follow-up was 12.5%, 14.5% 18%, and 23% in women, respectively, vs 9%, 10.5%, 12%, and 15%, respectively, in men (p=ns through year 3, p<0.05 thereafter). After multivariate analysis, gender was no independent risk factor of increased mortality. Major cardiac events and need for target vessel revascularization were unrelated to gender. CONCLUSIONS: There are no gender-specific differences in mortality after direct PTCA for acute myocardial infarction.

[Prevalence and significance of coronary collateral circulation in patients with acute myocardial infarct]. / Prävalenz und Bedeutung der koronaren Kollateralzirkulation bei Patienten mit akutem Myokardinfarkt.

UNLABELLED: Angiograms from consecutive and unselected patients with acute myocardial infarction were studied with respect to the prevalence as well as the significance of coronary collateral circulation to myocardium distal to the acute coronary occlusion. METHODS: Coronary angiograms were obtained from 700 consecutive and unselected patients with an acute transmural infarction within 3.7 +/- 3 hours (0.5-12) of symptom onset. No patient had undergone i.v. thrombolysis prior to angiography. Complete and acute vessel occlusion was found in 626/700 patients (89%). Coronary collaterals were detected and graded using Rentrop's classification. The grade of collateral circulation was related to the clinical course after 30 days and to the global and regional left ventricular wall motion. RESULTS: Collaterals were found in 334 patients (69%); 242 patients (38%) had collateral flow grade 2 or 3. Collaterals were demonstrated more frequently in women vs men and in patients with multivessel disease. The prevalence of collaterals was unrelated to age and the presence of diabetes mellitus. Patients who had angiography within 3 hours of symptom onset had collaterals detected less frequently than patients who had angiography beyond 6 hours (66% vs 75%, p < 0.05). No collaterals were found in 17/37 patients (47%) in cardiogenic shock and inferior MI but in only 30/164 patients (18%, p < 0.01) without shock. Global and regional left ventricular wall motion after 2 weeks was unrelated to the degree of coronary collateral circulation during acute myocardial infarction. CONCLUSION: Collateral circulation to myocardium distal to an acutely occluded coronary artery is detected in 2/3 patients during the acute infarct phase. The absence of collaterals is related to the early occurrence of cardiogenic shock in patients with inferior MI but not to the presence of diabetes mellitus. After direct angioplasty of the infarct vessel, the protective effects of coronary collaterals on chronic LV function remain uncertain.