Slight ST-segment Elevation Research Articles

The de Winter Pattern as Pre-Anterior ST-Elevation-Myocardial-Infarction. “An Evolution Sequence”: A Case Report

Introduction: The de Winter pattern (dWP) was first described by de Winter and colleagues in 2008 as static pattern associated with anterior myocardial infarction. A recent study showed the evolution sequence of this pattern into typical ST-elevation myocardial infarction (STEMI). This case discussed dWP who present as pre-anterior STEMI.
 Case Illustration: A-56-year old Male arrived in the emergency room complained chest pain about 3 hours. The patient also complained of diaphoresis, nausea, and fatigue. The patient has a previous history of hypertension. The vital signs were stable with an unremarkable physical examination. The initial electrocardiogram (ECG) revealed sinus rhythm with j-point depression followed by prominent T wave in precordial leads, slight ST-segment elevation in aVR, and loss of precordial R-wave progression. The initial-troponin-T was 31 pg/mL. Follow-up 1-hour after initial ECG showed typical ST-segment-elevation in V1-V4. The patient undergoing thrombolytic, followed by angiography that showed subtotal occlusion in the proximal left anterior descending (LAD) artery, occlusion in the proximal circumflex artery and stenosis in proximal right coronary artery, echocardiography revealed regional wall motion abnormality in the septal and anterior segments and preserved ejection fraction 58%, the patient was discharged after 8-days treated in intensive cardiac care unit.
 Conclusion: dWP has been shown as static and dynamic pattern in some conditions and associated with acute LAD occlusion. In this case, we showed dWP as early anterior STEMI, recognition of this pattern lead to early reperfusion and better myocardial salvage as anterior STEMI has a poor outcome.

A Novel Heterozygous Variant in F2 Gene in a Chinese Patient With Coronary Thrombosis and Acute Myocardial Infarction Leads to Antithrombin Resistance.

Thrombophilia refers to a group of conditions where the blood clots more easily than normal. These blood clots can cause problems such as deep vein thrombosis or pulmonary embolism. Most kinds of mutated coagulation factors II (F2) exhibit lower procoagulant activity, but in some cases, a higher coagulation rate has been observed. The underlying mechanism is that those variations can prevent F2s from being inhibited by antithrombin, leading to a contiguous activation of procoagulation, and causing recurrent thromboembolism. In this study, a patient was admitted to our hospital due to repeated chest pain for 2 days and aggravated for 4 h. A medical history investigation showed that he had three deep venous thromboses in the lower limbs and one portal vein thrombosis events during the past 10 years. The electrocardiogram showed Q wave elevation and slight ST segment elevation in lead V2, and coronary angiogram showed a total occlusion of the left anterior descending artery. Laboratory testing found that troponin I was obviously elevated. Family history also indicated that both his father (II-3) and grandfather (I-1) died from pulmonary thromboembolism. Whole-exome sequencing was performed to detect the genetic lesion of the patient, and a novel mutation (c.1621 C>T/p.R541W) of F2 was identified in the patient. This novel mutation resulted in a substitution of arginine by tryptophan, leading to antithrombin resistance (ATR). Our study is consistent with previously published papers. In conclusion, this study not only identifies a novel mutation of F2 and will contribute to the genetic diagnosis and counseling of families with thrombosis but also suggests that the site p.R541 of F2 may play a crucial role in thrombosis.

Mesalamine-induced myocarditis following diagnosis of Crohn's disease: A case report

Mesalamine is a common treatment for Crohn's disease, and can be rarely associated with myocarditis through a mechanism of drug hypersensitivity. We present the case of a 19-year-old male who developed chest pain two weeks after beginning mesalamine therapy. The electrocardiogram showed slight ST-segment elevation with upward concavity in the inferolateral leads; blood tests demonstrated elevated troponin I and the echocardiogram revealed moderately depressed left ventricular systolic function with global hypocontractility. Cardiac magnetic resonance imaging confirmed the diagnosis of myocarditis, revealing multiple areas of subepicardial fibrosis. The onset of symptoms after mesalamine, and improvement of chest pain, cardiac biomarkers and left ventricular systolic function after discontinuing the drug, suggest that our patient suffered from a rare drug-hypersensitivity reaction to mesalamine.

Mesalamine-induced myocarditis following diagnosis of Crohn's disease: A case report

Mesalamine is a common treatment for Crohn's disease, and can be rarely associated with myocarditis through a mechanism of drug hypersensitivity. We present the case of a 19-year-old male who developed chest pain two weeks after beginning mesalamine therapy. The electrocardiogram showed slight ST-segment elevation with upward concavity in the inferolateral leads; blood tests demonstrated elevated troponin I and the echocardiogram revealed moderately depressed left ventricular systolic function with global hypocontractility. Cardiac magnetic resonance imaging confirmed the diagnosis of myocarditis, revealing multiple areas of subepicardial fibrosis. The onset of symptoms after mesalamine, and improvement of chest pain, cardiac biomarkers and left ventricular systolic function after discontinuing the drug, suggest that our patient suffered from a rare drug-hypersensitivity reaction to mesalamine.

Massive Pericardial Effusion in a Case of Acute Pericarditis with Slight ST-Segment Elevation of Short Duration

We present the case of a 77-year-old woman who suffered from chest pain. Her white blood cell count was 10,200/μL and C-reactive protein level was 5.5 mg/dL. There was no electrocardiogram abnormality up to 5 hours after admission. At 15 hours, slight ST-segment elevation occurred, but this disappeared on day 4. Imaging revealed slight pericardial effusion. Nonsteroidal anti-inflammatory drugs and antibiotics were administered. However, the pericardial effusion, inflammatory response, and bilateral heart failure worsened. Pericardiotomy on day 6 released 350 mL of fluid, and symptoms improved. Viral pericarditis was assumed. Massive pericardial effusion is rare in cases of acute viral pericarditis, as is slight, short-duration ST-segment elevation.

When you hear hoofbeats, think of horses and zebras: a 58-year-old man with chest pain and palpitations

Case presentation and primary diagnosisDr. Szkodzinski, Dr. Nowowiejska-Wiewiora: A 58-year-old man presented to the emergency department (ED) withchest pain and palpitations of 2 h duration as well as arapid heart rate (approximately 170 beats/min) and dizzi-ness. The patient reported episodic palpitations within theprior 12 months. His past medical history was negativefor prior surgeries, medications or any drug allergies. Onadmission, the patient was normotensive, normocardicand afebrile. Physical examination was unremarkable. Anelectrocardiogram (ECG) showed a normal sinus rhythmwith slight ST-segment elevation in precordial leads V1and V2, and a rsr’ pattern in V1 (Fig. 1a). Laboratory testsrevealed elevated cardiac marker CK-MB mass 20 ng/mL(upper limit of normal 5 ng/mL) and troponin T 0.4 ng/mL(upper limit of normal 0.1 ng/mL). Based on the clinicalpresentation, elevated cardiac markers and ECG findings, aprimary diagnosis of ST-segment elevation myocardialinfarction (STEMI) was made. The patient received5,000 U of unfractionated heparin IV, 300 mg of aspirinand 600 mg of clopidogrel, and was transferred to cathe-terization laboratory.Final diagnosisDr. Hudzik, Dr. Wozniak: Coronary angiography showednormal coronary arteries. The ECG tracing normalizedafter the procedure (Fig. 1b). Echocardiography revealednormal left and right ventricle functions (left ventricularejection fraction 60%) with no structural heart disease.Inflammatory states were excluded based on negativeinflammation markers [high-sensitivity C-reactive protein0.9 mg/L, erythrocyte sedimentation rate 6 mm/h, normalleukocyte count 6.7 (10

Coronary Artery Spasm as a Cause of Droperidol-Induced Ventricular Fibrillation

To the Editor: Droperidol has been scrutinized for its potential arrhythmogenicity (1). This report describes a case of coronary artery spasm as a possible cause of droperidol-induced ventricular fibrillation. A 60-yr-old man with no history of cardiac disease underwent ileocecectomy to treat ileocecal lymphoma. He was receiving no medications, and was healthy other than the lymphoma. His preoperative 12-lead electrocardiogram showed QT prolongation with a QTc of 452 ms. Anesthesia was induced with 4.0 mg midazolam, 0.5 mg atropine, 200 μg fentanyl citrate, and 12 mg vecuronium bromide, and maintained with 50% NO2. One and a half hours after the start of surgery, we administered droperidol of 1.0 mg IV as prophylaxis for postoperative nausea and vomiting. Within a few minutes, the patient developed ventricular fibrillation (Fig. 1) with a torsade de pointes pattern, which subsided after electrical cardioversion at 200 J. Subsequent monitoring showed ST segment depression. Twelve-lead electrocardiogram approximately 5 min after defibrillation showed slight ST segment elevation in the inferior limb leads, and increased QTc of 463 ms. The ST segment elevation returned to baseline in several minutes. His electrolytes were normal: sodium 142 mEq/L, potassium 3.7 mEq/L, and calcium 7.8 mg/dL. The surgery was completed without complication, using IV lidocaine hydrochloride.Figure 1.: Ventricular fibrillation suddenly occurred a few minutes after an IV injection of 1.0 mg droperidol.On postoperative day 5 the patient underwent cardiac catheterization. Coronary angiograms showed no significant stenosis, but intracoronary injection of 10 μg ergonovine maleate provoked total obstruction of the middle right coronary artery segment (Fig. 2), accompanied by inferior ST segment elevations and polymorphic premature ventricular contractions.Figure 2.: Angiograms showed no significant stenosis in the native coronary arteries. The intracoronary injection of ergonovine maleate provoked occlusive spasm in the right coronary artery (allow).Torsade de pointes was temporally associated with droperidol, but was it caused by droperidol? Myocardial ischemia due to coronary artery spasm likely played a role in inducing ventricular fibrillation (2). Droperidol has been reported to enhance the effect of dopamine by blocking γ-aminobutyric acid receptors on the postsynaptic membrane (3). Dopamine may provoke coronary artery spasm (4), as does ergonovine maleate. Crea et al. (4) administered dopamine to 18 patients with active vasospastic angina. Half of the subjects developed angina and ischemic electrocardiographic changes suggestive of coronary spasm. Thus, one mechanism might be droperidol enhancement of coronary artery spasm. QT prolongation has been considered to be a risk factor for the development of the life-threatening ventricular arrhythmias (5), especially in the case of droperidol administration (1). Our patient showed a mild QT prolongation before surgery and after defibrillation. QTc was not measured strictly immediately after droperidol administration. Lischke et al. (6) studied serial electrocardiograms after injection of droperidol, demonstrating dose-dependent increase in QTc intervals. In isolated guinea pig ventricular myocytes, droperidol lengthened cardiac repolarization by blocking the rapid component of the delayed rectifier potassium current (7). In rabbit Purkinje fibers, droperidol induced early depolarizations and triggered activity (8). Thus, the heart may have been rendered more susceptible to arrhythmia from the coronary spasm, and thus more prone to droperidol-induced torsade. There are two mechanisms that potentially link the administration of droperidol to the onset of ventricular fibrillation with a torsade de pointes pattern. However, we cannot know whether the temporal association was causal or just coincidental. Nobuyuki Miyai, MD Tatsuya Kawasaki, MD, PhD Hiroki Sugihara, MD, PhD Department of Cardiology Ryotaro Kayo, MD Department of Anesthesiology Matsushita Memorial Hospital Osaka, Japan [email protected]

Inverted T Wave Returning to Upright During Acute MI

A 70-year-old man was seen in the emergency department for severe substernal chest pain that had become progressively worse during the past 48 hours. The initial ECG showed pathological Q waves and T-wave inversion in leads I and aVL, with only slight ST segment elevation. He was hospitalized and found to have elevated creatine kinase levels that peaked at 3,360 mU/mL. On hospital day 3, cardiac catheterization showed total occlusion of the left anterior descending artery and severe stenosis at the origin of a large ramus intermedius artery. Because of the unfavorable anatomy and presumed long interval since onset, no coronary intervention was performed.Several days later the patient complained of a new type of chest pain that involved primarily the left shoulder. A pericardial friction rub was noted, and a rapid irregular rhythm began. The ECG is shown.

Acute MI with Subsequent Heart Murmur

A 67-year-old woman was seen in the emergency department for severe substernal chest pain that had begun suddenly 12 hours earlier. The ECG showed slight ST-segment elevation in the inferior leads and ST-segment depression in the anteroseptal leads. There was no relief from nitroglycerin given sublingually and only partial relief from nitroglycerine administered intravenously. The patient declined both thrombolytic therapy and immediate cardiac catheterization.During observation over the next 12 hours, she had continuing chest discomfort and required a total of 25 mg of morphine sulfate. The creatine kinase level rose to a peak of 2,275 U/L. Examination the next morning showed an elderly woman in moderate respiratory distress. Blood pressure was 110/70 mm Hg; pulse, 110 beats per minute and regular; respirations, 26 per minute; temperature, 37.9°C; and arterial oxygen saturation, 93% on nasal oxygen at 2 L/min. With the patient seated, jugular venous pressure was elevated to the angle of the jaw There were crackles throughout the lung fields. Cardiac examination showed a grade 4 holosystolic murmur at the apex, radiating to the axilla, with a prominent S3. (The murmur had not been noted in the initial evaluation, and there was no history of a heart murmur.) The ECG taken the morning after admission is shown.

ST segment and T wave characteristics as indicators of coronary heart disease risk: The Zutphen study

This study evaluated the predictive value of T wave amplitude and ST segment level on lead I for angina pectoris, a first myocardial infarction, sudden death and coronary heart disease death in middle-aged and elderly men. Certain ST-T wave characteristics may reflect favorable autonomic cardiac control. Slight ST segment elevation has been reported to indicate a low risk of coronary heart disease mortality. A total of 876 men, born between 1900 and 1920, participated in periodic medical examinations and were followed up with respect to morbidity and mortality from 1960 to 1985. In 1985, the remaining cohort was extended to 836 elderly men from the same birth cohort who were followed up until 1990. Relative risks in categories of T wave amplitude and ST segment level were estimated by survival analysis. Both middle-aged and elderly men with T wave amplitudes > or = 0.15 mV had a lower risk of myocardial infarction, coronary heart disease death and sudden death than men with T wave amplitudes 0.05 to 0.15 mV. The adjusted relative risk of coronary heart disease death was 0.5 (95% confidence interval [CI] 0.2 to 1.0); in men with T wave amplitude < or = 0.05 mV, relative risk was 2.0 (95% CI 1.3 to 3.1). Slight ST segment elevation was also associated with decreased risk: relative risk 0.5 (95% CI 0.3 to 1.0) compared with the isoelectric ST segment level. In men with ST segment depression, relative risk was 2.2 (95% CI 1.4 to 3.4). The association of T wave amplitude and ST segment level were independent of each other. In addition to the elevated risk of coronary heart disease that is associated with ST-T wave abnormalities, we observed that normal variations in repolarization characteristics are predictive of future heart disease.

Extent of early ST segment elevation resolution: A simple but strong predictor of outcome in patients with acute myocardial infarction

Objectives. This study proposed to verify the prognostic power of early ST segment elevation resolution in patients with acute myocardial infarction from the Intravenous Streptokinase in Acute Myocardial Infarction study data base.Background. Data from a small prospective study suggested that use of two cutoff points for three different levels of ST segment resolution 3 h after the start of thrombolysis may be an efficient way to predict outcome in an individual patient.Methods. The three groups of ST segment resolution were defined as 1) complete resolution (≥70% [552 patients]) or only slight ST segment elevation (127 patients); 2) partial resolution <70% to 30% [475 patients]); 3) no resolution (<30% to >0% [362 patients]). Infarct size was measured from creatine kinase isoenzyme, MB fraction, release and from the number of Q waves. Left ventricular function was assessed In 818 patients 1 month after infarction.Results. For complete, partial and no ST segment resolution 3 h after the start of streptokinase or placebo infusion, enzyme release was 1.2, 1.8 and 2.1 IU/ml × h; number of Q waves 1.7, 2.5 and 3.0; and ejection fraction 60%, 53% and 49%, respectively (all adjusted p = 0.0000). Mortality rate at 21 days was 2.2%, 3.4% and 8.6%, respectively. No ST segment resolution was the most powerful independent predictor of early mortality (p = 0.0001). Survival rate curves at 6-year follow-up showed significant mortality differences with increasing divergence (p = 0.0003 anterior infarction; p = 0.005 inferior infarction). In subgroups with an overall higher risk of dying, mortality was strongly determined by the extent of early ST segment resolution.Conclusions. The extent of ST segment elevation resolution conveys useful early information about outcome in an individual patient after acute myocardial infarction.

Sudden death in primary mitral valve prolapse

Sudden unexpected death is a recognized complication of mitral valve prolapse (MVP), but well-documented cases are rare and either clinical details or necropsy findings are absent or scanty. One of our patients, a young woman with MVP who had been fully investigated’e2 and followed since childhood, died suddenly at the age of 24 years, and we were able to obtain detailed pathologic findings. At the age of 8 years a grade 216 late systolic murmur and a nonejection click were heard (see Fig. 10 of Ref. 1). Occasional ectopic beats were present, but she was asymptomatic. Chest x-ray examination was normal. The ECG (see Fig. 11 of Ref. 1) showed slight ST segment elevation with T wave inversion in leads 2, 3, and AVF. Left ventricular cineangiography (see Fig. 12 of Ref. 1) demonstrated mild mitral regurgitation and marked prolapse of the posterior leaflet. Her father had an isolated nonejection click. A diagnosis of MVP on a familial basis was made, and no treatment was given. She attended the clinic at B-month intervals and remained asymptomatic. At 13 years of age numerous multifocal ventricular premature contractions were recorded after a strenuous exercise test (See Fig. 2, a of Ref. 2). On propranolol, 80 mg daily, and diphenylhydantoin, 300 mg daily, the arrhythmia was suppressed. She was thereafter assessed at yearly intervals