Impending Myocardial Infarction Research Articles

Abstract 14284: "Weeding" Out Wellens' Syndrome

Introduction: Wellens’ syndrome, most often associated with proximal left anterior descending coronary artery stenosis, is considered highly specific for impending myocardial infarction (MI). Its diagnosis relies on symmetric biphasic or deeply inverted T waves in leads V1-V4, normal precordial R wave progression and normal to slightly elevated cardiac markers. Pseudo-Wellens’ syndrome presents similarly, but in the absence of coronary artery disease (CAD). We present a challenging case of a patient with history of excessive recreational cannabis use and incidental electrocardiogram (ECG) findings concerning for Wellens’ syndrome who ultimately was diagnosed with Pseudo-Wellens’ syndrome. With familiarity of cannabis associated Pseudo-Wellens’ syndrome, unnecessary invasive diagnostic and therapeutic procedures were avoided. Case: A 20 year old male without significant past medical history presented for evaluation of vomiting and abdominal pain of 2 days duration. In view of his daily cannabis use, he was diagnosed with cannabis hyperemesis syndrome. An ECG to measure QTc prior to administration of ondansetron demonstrated ST elevation in lead V2. A repeat ECG showed T-wave inversions in leads V2-4. Troponin levels were negative. The patient denied chest pain or shortness of breath. An echocardiogram showed normal cardiac wall motion and an estimated ejection fraction of 55-60%. The diagnosis of Pseudo-Wellens’ syndrome secondary to cannabis use was made and the patient was subsequently discharged home following extensive cannabis cessation counseling. Discussion: The definitive treatment of Wellens’ Syndrome relies on cardiac catheterization even in patients without cardiac history or risk factors for CAD. This immediate intervention is required to halt the evolution of MI and is crucial for a positive outcome. In contrast, Pseudo-Wellens’ syndrome occurs in the absence of CAD and has been reported in younger, healthy patients in association with illicit drug use. In the era of increased legalized marijuana use, it is imperative that health care providers are familiar with cannabis induced Pseudo-Wellens’ syndrome as to avoid the potential for inappropriate invasive diagnostic modalities in otherwise healthy individuals.

CRYPTIC CHEST PAIN: WELLEN’S SYNDROME DUE TO MYOCARDIAL BRIDGING

SESSION TITLE: Cardiovascular Disease 2 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Chest pain of cardiac origin is commonly ischemic in etiology. However, the phenomenon of myocardial bridging as a cause of chest pain has come to attention recently. Herein, an epicardial coronary artery develops a transient myocardial course. During systole, a portion of the vessel is mechanically compressed and results in ischemia. This has been attributed to as a rare cause of angina. Here we present our experience with a patient who was diagnosed with the same. CASE PRESENTATION: A 51 year old man with no past medical history, presented to the emergency room with pressure like chest pain of two days duration. He had multiple episodes of pain and each lasted for around 20 minutes. It was associated with palpitations, and exacerbated by physical exertion. He was a former smoker and reportedly quit smoking 20 years back. His blood pressure was 153/95 mmHg; temperature 98.1F; heart rate 73/min regular; respiratory rate 18/min. ECG showed Type 1 Wellen's biphasic pattern in V2, V3. Three sets of cardiac troponins were normal. Wellens pattern on ECG is highly specific (89%) for critical left anterior descending artery (LAD) stenosis. [1] [2]. Therefore, the patient was sent for emergent cardiac catheterization. Coronary angiography revealed normal left main, left circumflex and right coronary artery. However, LAD artery showed moderate myocardial bridging. DISCUSSION: In myocardial bridging, a coronary artery that normally runs on the epicardium, develops a transient intra-myocardial course. This section of the artery gets compressed during ventricular systole. Generally asymptomatic, bridging sometimes results in angina, arrhythmias myocardial ischemia. Most myocardial bridging has been found to occur in the middle portion of the LAD artery. However, on autopsy right coronary and left circumflex arteries have shown bridging at comparable rates. [3]. Proximal portion of the bridged segment is prone to accelerated atherosclerosis.Hypertrophic obstructive cardiomyopathy (HOCM) has shown increased association with myocardial bridging. Treatment is with beta blockers and non-dihydropyridine calcium channel blockers. Therapeutic benefit results from decreased chronotropy and inotropy. In cases refractory to medical management, surgical myotomy, coronary artery stenting or coronary artery bypass grafting (CABG) can be pursued. Our patient was started on aspirin, amlodipine, metoprolol, and rosuvastatin. His hospital course was uneventful and he was discharged on pharmacological therapy. CONCLUSIONS: Myocardial Bridging is being recognized increasingly as a cause of refractory angina. However, it is still not widely included as a differential diagnosis. Since the treatment is fairly specific, we wish to underscore the importance of recognizing myocardial bridging as an atypical cause of chest pain. Reference #1: C. de Zwaan, F.W. Bar, H.J. Wellens. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J, 103 (1982), pp. 730-736. Reference #2: C. de Zwaan, F.W. Bar, J.H. Janssen, et al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. . Am Heart J, 117 (1989), pp. 657-665. Reference #3: Polacek P, Kralove H. Relation of myocardial bridges and loops on the coronary arteries to coronary occlusions. Am Heart J. 1961;61:44-52 DISCLOSURES: No relevant relationships by Paurush Ambesh, source=Web Response No relevant relationships by Stephan Kamholz, source=Web Response No relevant relationships by Dikshya Sharma, source=Web Response No relevant relationships by Ankur Sinha, source=Web Response

Wellens syndrome in HIV-infected patients

Background:Wellens syndrome is a pattern of electrocardiographic (ECG) changes in the context of unstable angina characterized with deep inverted T-waves or biphasic T-waves in the precordial leads. These specific ECG changes are highly suggestive of stenosis in the left anterior descending artery (LAD), which can result in acute myocardial infarction, left ventricular dysfunction, or death. Human immunodeficiency virus (HIV) infection is known as an independent risk factor for the cardiovascular disease.Case Report:The first case is a 61-year-old African American female with a history of HIV infection who presented with chest pain for 8 h. Electrocardiogram (ECG) showed deep T-waves inversions in leads V3–V6. Emergent cardiac catheterization showed 99% stenosis in the mid-LAD and a drug-eluting stent (DES) was subsequently placed. The second case is a 49-year-old African American female with a medical history of type 2 diabetes mellitus, HIV, active cigarettes smoker admitted for intermittent substernal chest pain of 1-day duration. ECG showed biphasic T-wave in V2 and deep T-waves inversion in V3–V4, coronary angiography showed 95% stenosis in the proximal LAD and a DES was placed.Conclusion:Wellens syndrome has characteristic ECG changes that indicates LAD stenosis. Early recognition of this syndrome, especially in HIV-infected patients who are high risk for cardiovascular disease, will help to avoid impending myocardial infarction.

‘Action potential-like’ ST elevation following pseudo-Wellens' electrocardiogram

Coronary artery vasospasm is an important cause of chest pain syndromes that can lead to myocardial infarction, ventricular arrhythmias, and sudden death. In 1959, Prinzmetal et al described a syndrome of nonexertional chest pain with ST-segment elevation on electrocardiography. Persistent angina is challenging, and repeated coronary angioplasty may be required in this syndrome. Calcium antagonists are extremely effective in treating and preventing coronary spasm, and may provide long-lasting relief for the patient. Whereas the Wellens' syndrome is characterized by symmetrically inverted T-waves with preserved R waves in the precordial leads suggestive of impending myocardial infarction due to a critical proximal left anterior descending stenosis, the pseudo-Wellens' syndrome caused by coronary artery spasm has also rarely been reported in literature. We present a pseudo-Wellens syndrome as a cause of vasospastic angina, and a diffuse ST segment elavation on electrocardiogram resembling the Greek letter lambda, called also 'action potential-like' ECG in a patient with vasospastic-type Printzmetal angina.

Slow Regular Rhythm in a Disoriented Patient

A 65-year-old woman with a history of high blood pressure, diabetes mellitus, hyperlipidemia, chronic kidney disease, and stroke went to a walk-in clinic complaining of intermittent neck, left shoulder, and arm pain for several days. After being diagnosed with pneumonia and started on antibiotics, the patient went home. The pain became worse and constant 2 days later, and several hours thereafter her family found her disoriented and diaphoretic. An electrocardiogram on hospital admission showed atrial fibrillation, complete atrioventricular block, and a regular junctional escape rhythm at a rate of 37 beats/min (Figure). QRS, ST, and T changes indicated acute inferoposterolateral myocardial infarction, and the QT interval was long (604 msec; QTc 562). Figure. Electrocardiogram recorded on hospital admission. See text for explication. A survey of 11 studies of the culprit lesion sites in acute inferior myocardial infarction found right coronary artery to left circumflex coronary artery ratios that ranged from 2.2:1 to 7.0:1 with a mean of 4:1 (1). Furthermore, the artery to the AV node is a branch of the right 90% of the time and of the left circumflex only 10% of the time. Thus, there are good reasons for suspecting the right coronary artery as the culprit. Two findings, however, are common in left circumflex occlusions, but uncommon in right occlusions: ST depression in both leads V1 and V2 and ST depression ≥0.1 mV (1 mm) in lead aVR (1). Coronary arteriography, the ultimate clinical arbiter, demonstrated atherothrombotic occlusion in the middle portion of a dominant left circumflex coronary artery. This was treated with a bare metal stent, and a temporary transvenous electronic ventricular pacemaker increased the rate to 60 beats/min. Serum troponin I peaked at 75 ng/mL; reference, <0.04 ng/mL. Unfortunately, although atrioventricular block decreased to second and then first degree over 2 days, the patient remained poorly responsive for 6 days, suffered transient kidney failure requiring hemodialysis, and had acute respiratory distress syndrome requiring endotracheal ventilation for 12 days. The prolonged intubation caused dysphagia necessitating total parenteral nutrition via a percutaneous indwelling central catheter. Thrombocytopenia, seemingly induced by eptifibatide, abated after the drug was stopped. After 4 weeks of hospitalization, the patient was well enough to be transferred to an inpatient rehabilitation facility. The electrocardiographic lesson is that because a dominant left circumflex coronary artery supplies not only the usual distribution of the left circumflex, but also most of the usual distribution of the right, occlusion of a dominant circumflex usually causes a large infarct that has electrocardiographic features of both circumflex and right occlusions. The more important lesson is that failure to recognize an impending myocardial infarction often results in a clinical catastrophe.

The sick LADy who cried wolf: A case of Wellens’ syndrome presenting in the shadow of chronic sickle cell pain

Abstract Introduction Chest pain is a common presenting complaint in the emergency centre (EC), with a very wide differential diagnosis. Evaluation of patients with chest pain in the EC is geared toward rapidly identifying and treating the subset of patients with potentially life-threatening causes, including acute coronary syndromes. ECG and cardiac biomarkers are indispensable tools in this endeavor. Case report A 47year old African woman presented to the EC with chest pain; her ECG revealed findings typical of Wellens' syndrome. Subsequent coronary angiography revealed near-total proximal LAD occlusion. Discussion Wellens' syndrome refers to a pre-infarction stage of acute coronary syndrome with distinct ECG T-wave changes that strongly predict the presence of critical LAD coronary artery stenosis; it is a harbinger of impending extensive anterior myocardial infarction. Emergency physicians must be able to recognize its ECG features and institute appropriate intervention.

A Rare Complication of Ulcerative Colitis: ST Elevation Myocardial Infarction

Purpose: A 44-year-old female presented to the emergency room (ER) with sudden onset substernal chest pain. The patient had no known cardiac risk factors. She had a history of Ulcerative Colitis (UC), which had been in remission until two days prior to the presentation, when she started having abdominal pain and bloody diarrhea. This episode was similar to her prior exacerbations but she was currently not on any treatment. The physical exam was only remarkable for mild diffuse tenderness in the abdomen. The EKG done in the ER showed ST segment elevations in leads II, III and aVF and the lab work was significant for elevated cardiac enzymes (Troponin I-25 ng/ml). The patient underwent an urgent cardiac catheterization which revealed total occlusion of the right coronary artery. The artery could not be stented due to the presence of extensive thrombus and even though, thrombectomy was attempted, it was not successful. The decision was made to manage the patient medically and she was started on a beta blocker, ACE inhibitor and statin for acute MI and mesalamine for Ulcerative colitis exacerbation. Aspirin and Clopidogrel were held in the light of bloody diarrhea but it was decided to start intravenous heparin. The patient responded well to the treatment. The hematocrit remained stable and there were no further episodes of bleeding. She was eventually discharged in a stable condition. Ulcerative colitis is frequently associated with many extra-intestinal manifestations, mostly in the form of dermatological, hepatobiliary or ocular involvement but cardiac involvement is rare. It usually manifests as either pericarditis with or without myocardial involvement or conduction abnormalities. Myocardial infarction, as seen in our patient, is an extremely rare complication of Ulcerative colitis. The hypercoagulable state in UC is postulated to be due to increased levels of platelets, prothrombin fragment, fibrinogen, homocysteine and reduced levels of anticoagulants. These alterations in the coagulation cascade can result in deep venous thrombosis, pulmonary embolism, atrial thrombi and rarely coronary artery thrombosis. Interestingly, intravenous heparin has been suggested as a treatment for UC exacerbation along with standard therapy, with no increase in the incidence of bleeding. The exact mechanism by which heparin ameliorates the exacerbation is still unclear but it makes it particularly beneficial in the setting of a MI. We would like to conclude that physicians should be aware of this rare complication of Ulcerative colitis and it is important to recognize chest pain during UC exacerbation as it can indicate an impending Myocardial Infarction.

Effects of HBOC‐201 in a porcine model of impending myocardial infarction produced by severe coronary artery stenosis

Hemoglobin oxygen carrier HBOC‐201 can act as a direct oxygen donor and facilitate diffusive oxygen delivery between red blood cells and tissues to improve tissue oxygenation. Recently we showed that pre‐oxygenated HBOC‐201 infused distal to a coronary occlusion, fully restored aerobic metabolism and myocardial function. Here, we studied the effects of systemic administration of HBOC‐201 on left ventricular (LV) function and infarct size (IS) in pigs with coronary stenosis. A stenosis placed in the left anterior descending coronary artery for 120 min reduced flow by 70±2%. HBOC‐201 (1 g/kg), with or without nitroglycerine (NTG), were infused iv over 30 min, starting 15 min after the onset of ischemia. After 120 min of reperfusion, the area‐at‐ risk (AR), infarct area (IA) and IS=IA/AR•100% were determined. HBOC‐201 did not ameliorate stenosis‐induced loss of regional systolic segment shortening (from 20±1% to −3±1%) in the anterior LV wall and had no effect on IS (33±5%) compared to control (39±5%). To balance the purported scavenging of nitric oxide by HBOC‐201, we co‐infused NTG during HBOC‐201 which prevented systemic and coronary vasoconstriction. However, even in the presence of NTG, HBOC‐201 failed to blunt regional dysfunction or reduce IS (40±6%). Thus, despite the established oxygen transport capacity of HBOC‐201, it failed to afford cardioprotection in the setting of ischemia‐reperfusion in pigs.

Establishment and Characterization of an Experimental Model of Coronary Thrombotic Microembolism in Rats

To establish a model of coronary thrombotic microembolism in rats, either automicrothrombotic particulates (CM group) or saline control (SHAM group) was injected into temporarily clamped aortas of male Sprague-Dawley rats. After automicrothrombotic particulate injection, serum c-troponin I and von Willebrand factor levels, the no-flow area as evaluated by Thioflavin S, myocardial leukocyte infiltration levels, myocardial expressions of tumor necrosis factor alpha and interleukin-6, the percentage of arterioles obstructed by thrombosis, and myocardial fibrosis were all significantly increased whereas cardiac function as evaluated by echocardiography and hemodynamic measurements were significantly reduced compared with the sham group. Thus, aortic automicrothrombotic particulate injection could induce coronary microembolism in rats, and this model could be of value in improving the understanding of pathophysiology of coronary microembolism.

An uncommon clinical picture: Wellens’ syndrome in a morbidly obese young man

A 39-year-old man presented to the emergency department (ED) of the ‘‘Paolo Giaccone’’ Academic Hospital, Palermo (Italy). He had anterior chest pain that did not radiate to the neck or arms. The patient came from home where the chest pain initiated. The patient was morbidly obese (BMI 54 kg/m). At the ED, the patient’s blood pressure was 120/80 mmHg, the serum troponin I concentration was 0.029 ng/ml (normal values 0.034, borderline 0.034–0.12), myoglobin 45 ng/ml (normal values 120). While experiencing chest pain, the patient underwent a standard 12 lead electrocardiogram (ECG) that was normal. An echocardiogram, also during the chest pain, excluded the presence of hypo-akinetic left ventricle areas. He was admitted to the internal medicine ward of the same hospital for clinical monitoring. Cardiac biohumoral markers were measured every 4 h, and were always within normal range (only troponin I reached 0.12 ng/ml falling to 0.028 ng/ml). On the following morning, anterior chest pain recurred. Another ECG was performed, but showed no abnormalities (Fig. 1a). During the afternoon, the patient underwent another ECG. He had no thoracic discomfort or pain, but the ECG showed a biphasic T wave inversion in V2–V6 precordial leads (Fig. 1b). Cardiac markers resulted again within normal range. An internal medicine resident who was trained to manage uncommon clinical pictures by PubMed searching [1] recognized this abnormal pattern (ECG abnormalities in an asymptomatic patient with prior anterior chest pain) performed a PubMed search using the following simple search string (biphasic T waves AND precordial leads). Six citations were found and Wellens’ Syndrome diagnosis was suggested. An internist confirmed the diagnostic hypothesis, and the patient, was taken to the invasive hemodynamic lab. Coronary arteriography was performed showing a 95% stenosis of the left anterior descending (LAD) coronary artery (Fig. 2a). The patient underwent percutaneous transluminal coronary angioplasty with resolution of the stenosis (Fig. 2b) and was discharged after 6 days in good condition. In 1982, Wellens et al. [2] described a characteristic ECG pattern associated with a critical stenosis of the LAD coronary artery and impending myocardial infarction. Tilkian [3] was the first to use the term Wellens’ syndrome defined as a group of ECG signs that occur during the painfree period in a patient with unstable angina. These ECG abnormalities, in the absence of pathologic Q waves, are predictive of a critical proximal LAD stenosis [2, 4]. They consist of an isolectric or minimally elevated ST segment followed by a concave or straight ST segment and symmetrically inverted (or biphasic) T waves in the precordial leads, frequently in V2–V3, but sometimes involving V4, V5 or V6. [4]. This was the case of our patients who showed a biphasic T wave inversion in V2–V6, leads during a pain-free period. In conclusion, this uncommon clinical picture involves one of the four clinical diagnostic strategies known as pattern recognition. This kind of diagnostic method particularly depends upon the experience of the physician. Nevertheless, we think this kind of clinical picture could be interpreted successfully using PubMed by a non-experienced physician [5]. S. Corrao (&) S. Amico L. Calvo E. Barone G. Licata Dipartimento Biomedico di Medicina Interna e Specialistica, Universita di Palermo, Piazza delle Cliniche, 2, 90127 Palermo, Italy e-mail: s.corrao@tiscali.it

Interaction Between Pre- and Postconditioning in the In Vivo Rat Heart

Patients with an impending myocardial infarction may be preconditioned by pre-infarct angina. Hence, it is important to establish whether ischemic postconditioning is still effective in preconditioned hearts. We therefore studied in anesthetized rats the effect of postconditioning after coronary artery occlusions (CAO) of 60 min in control hearts, hearts preconditioned by a single 15-min CAO (1IPC15) or a triple 3-min CAO (3IPC3). Furthermore, we studied the effect of postconditioning in hearts that had been pharmacologically preconditioned with intravenous adenosine and in hearts that had become tolerant to 1IPC15. Postconditioning limited infarct size in control hearts, but did not afford additional protection in preconditioned hearts, irrespective of the IPC stimulus. NO synthase inhibition abolished the cardioprotection by postconditioning, both IPC stimuli, and the combination of postconditioning and either IPC stimulus. Postconditioning also failed to afford cardioprotection in hearts protected by adenosine, and in hearts that had become tolerant to cardioprotection by 1IPC15. In accordance with previous observations, postconditioning paradoxically increased infarct size following a 30-min CAO. This detrimental effect was prevented by either IPC stimulus, in a NO synthase-dependent manner. In conclusion, postconditioning does not afford additional protection in preconditioned hearts, irrespective of the preconditioning stimulus and the presence of tolerance to preconditioning. Lack of additional protection may be related to the observation that postconditioning and preconditioning are both mediated via NO synthase. In contrast, the increase in infarct size by postconditioning following a 30-min CAO is abolished by either IPC stimulus. These findings indicate that the interaction between preconditioning and postconditioning is highly dependent on the duration of index ischemia, but independent of the preconditioning stimulus.

Pseudo Wellens T-waves in patients with suspected myocardial infarction: How cardiac magnetic resonance imaging can help the diagnosis

Wellens' syndrome is characterized by symmetrically inverted T-waves in the precordial leads suggestive of impending myocardial infarction due to a critical proximal left anterior descending (LAD) stenosis. We describe three unusual cases of patients with such electrocardiographic abnormality in which coronary angiography ruled out the presence of critical coronary stenosis and cardiac magnetic resonance imaging excluded the presence of acute or chronic myocardial infarction.

Coronary Stenting During Burn Shock: Diagnostic and Treatment Considerations

Myocardial injury is known to occur in victims of both thermal and electrical burns. A variety of mechanisms have been ascribed to the pathogenesis of cardiac damage during burn shock. However, limited evidence exists that coronary artery thrombosis plays a frequent role. Distinguishing between acute coronary syndrome (impending myocardial infarction from coronary artery occlusion) vs global cardiac injury is essential; the care diverges drastically. The following case describes a patient who was angiographically proven to have acute coronary thrombosis amidst burn shock ftera 50% TBSA electrical flash burn. Managing the patient's burn shock, myocardial injury, and multiple surgical procedures while considering antiplatelet medications for a newly placed coronary artery stent presented a number of challenges not previously reported.

Coronary microembolization

Atherosclerotic plaque rupture is the key event in the pathogenesis of acute coronary syndromes and it also occurs during coronary interventions. Atherosclerotic plaque rupture does not always result in complete thrombotic occlusion of the epicardial coronary artery with subsequent impending myocardial infarction, but may in milder forms result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation. This review summarizes the present experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes and highlights the main consequences of coronary microembolization--reduced coronary reserve, microinfarction, inflammation and oxidative modification of contractile proteins, contractile dysfunction and perfusion-contraction mismatch.Furthermore, the review presents the available clinical evidence for coronary microembolization in patients and compares the clinical observations with observations in the experimental model.

Is apoptosis a diagnostic marker of acute myocardial infarction?

To investigate and quantify the presence of apoptosis in early myocardial ischemia in humans. Histologic sections from the left and right ventricles of 16 hearts with impending myocardial infarction were stained with terminal deoxynucleotidyl transferase-mediated deoxyuridine 5-triphosphate nick end labeling (TUNEL) method and with antibodies to p53, bcl-2, cpp32, FAS, FAS-L, and bax. DNA electrophoretic analysis was also performed. According to the inclusion criteria, all 16 cases showed morphologic changes consistent with ischemia and/or reperfusion. TUNEL results were positive in 14 of the 16 ischemic areas. Unexpectedly, they were also positive in "remote from ischemia" myocardium of both the left and right ventricles. DNA electrophoretic analysis confirmed the results of TUNEL. Immunohistochemistry was uniformly negative, probably because of autolysis phenomena. We showed that apoptosis precedes necrosis in humans, but the detection of apoptosis cannot be used as a diagnostic tool, since it can also be triggered by nonischemic events.

Is apoptosis a diagnostic marker of acute myocardial infarction? An autopsy study comparing histologic, immunohistochemical, tunel, and DNA electrophoresis evidence

Abstract Objective.—To investigate and quantify the presence of apoptosis in early myocardial ischemia in humans. Methods.—Histologic sections from the left and right ventricles of 16 hearts with impending myocardial infarction were stained with terminal deoxynucleotidyl transferase–mediated deoxyuridine 5-triphosphate nick end labeling (TUNEL) method and with antibodies to p53, bcl-2, cpp32, FAS, FAS-L, and bax. DNA electrophoretic analysis was also performed. Results.—According to the inclusion criteria, all 16 cases showed morphologic changes consistent with ischemia and/or reperfusion. TUNEL results were positive in 14 of the 16 ischemic areas. Unexpectedly, they were also positive in “remote from ischemia” myocardium of both the left and right ventricles. DNA electrophoretic analysis confirmed the results of TUNEL. Immunohistochemistry was uniformly negative, probably because of autolysis phenomena. Conclusions.—We showed that apoptosis precedes necrosis in humans, but the detection of apoptosis cann...

Surgical treatment of acute myocardial infarction

The development of direct coronary artery surgery by the saphenous vein graft technique for the first time provides a method that immediately increases the supply of oxygen to the myocardium. As a result, the area of myocardial infarction no longer depends only upon oxygen consumption. Emergency surgery was performed on 29 patients from April 1968 to May 1971; 18 operations were performed upon patients with impending myocardial infarction and 11 upon patients with acute myocardial infarction. Nineteen patients underwent coronary cineangiography before the acute episode; 9 were studied during an acute episode. Patients with impending myocardial infarction were operated on within 24 hours of the acute episode. Nine patients with acute infarction were operated upon within 4 to 5 hours, 1 within 8 hours and 1 within 10 hours. Three patients died after the operation; 2 in the group with impending myocardial infarction and 1 in the group with acute infarction. Twelve patients underwent repeat cineangiographic evaluation. All grafts but 1 were open. In the group with impending myocardial infarction, postoperative left ventriculography showed good function of the left ventricle. In the group with acute myocardial infarction, 4 patients showed good function of the left ventricle. In 1 the ventricle was unchanged, and in 2 impaired contraction was demonstrated. Although the present clinical experience is limited, certain conclusions can be made: (1) Emergency coronary cineangiography can be performed with minimal risk. (2) Patients with impending myocardial infarction can undergo operation with a low mortality rate and minimal complications. These patients are ideal candidates. The operation can prevent myocardial infarction. (3) When operations are performed within 6 hours of an acute myocardial infarction, most of the heart muscle can be preserved. (4) In patients with acute myocardial infarction and cardiogenic shock, assisted mechanical circulation is mandatory as the first step. The increase of well-oxygenated blood supply should improve myocardial perfusion.

Impending acute myocardial infarction during severe exercise associated with a myocardial bridge

Impending acute myocardial infarction during severe exercise associated with a myocardial bridge

Xiphodynia masking acute myocardial infarction: A diagnostic cul-de-sac

A 52-year-old hypertensive woman is described in whom a clinically evident diagnosis of xiphodynia, the painful xiphoid process, complicated the diagnosis of impending myocardial infarction. The authors suggest that xiphodynia be considered a second-line assumption after more dangerous conditions have been thoroughly ruled out.

Long-term results of emergency coronary artery bypass grafting.

During a 20-year period, 364 patients underwent coronary artery bypass grafting (CABG) for the treatment of ischemic heart disease. Among these patients, 28 underwent emergency surgery. The reasons for performing emergency CABG were unstable angina in 15 patients, impending myocardial infarction in 12 patients and congestive heart failure in 1 patient. Eleven patients died postoperatively. Eight variables were examined by univariate analysis for their influence on the occurrence of a hospital death. Lack of a history of myocardial infarction, intraaortic balloon pumping (IABP) and acute coronary occlusion were all found to be predictors of hospital death. Seventeen patients were followed up for 12 years. There was no cardiac death and actuarial survival at 12 years was 63%. The 14 survivors are now in NYHA functional class I or II. Although the operative mortality rate is high after emergency CABG, a fair prognosis can be expected if the patients survive surgery.