ST-segment Elevation In Electrocardiogram Research Articles

Subacute thrombosis after primary percutaneous coronary intervention with bioresorbable vascular scaffold implantation

Everolimus-eluting bioresorbable vascular scaffold (BVS) is a promising new technology recently applied in the treatment of coronary artery lesions that might overcome the limitations of the currently used drug eluting stents. There were no scaffold thromboses reported in the first-in-human trials with BVS implantation. However, the current body of evidence on its safety and incidence of early thrombotic complications in the setting of acute coronary syndromes is still limited. We present the case of a 58-year-old male who was admitted to a coronary care unit due to typical (two-hour long) chest pain with electrocardiographic signs of anterior wall ST segment-elevation myocardial infarction. Coronary angiography revealed critical stenosis of the proximal left anterior descending artery (Fig. 1A). Subsequent primary angioplasty with manual aspiration thrombectomy, balloon predilatation, and implantation of BVS (ABSORB, 3.5/28 mm, 12 atm.) was performed, with good angiographic result (TIMI 3 flow) (Fig. 1B). Optical coherence tomography (OCT) confirmed good scaffold expansion and complete strut apposition (Fig. 1C–F). Further in-hospital course was uneventful and the patient was discharged after five days of hospitalisation. On the ninth day after BVS implantation he presented again with acute severe chest pain and anterior ST-segment elevation in electrocardiogram. The patient confirmed that he discontinued both antiplatelet drugs (aspirin and clopidogrel) after discharge. Repeat coronary angiography revealed a subacute scaffold thrombosis (Fig. 2A). Manual aspiration thrombectomy, abciximab infusion, and plain old balloon angioplasty was performed (Fig. 2B), with good final angiographic result (TIMI 3) (Fig. 2C). Echocardiography revealed an impaired left ventricular ejection fraction of 38%, compared to 50% directly after the primary index procedure. As there was appropriate scaffold expansion and strut apposition in OCT directly after the index procedure, the most likely cause of scaffold thrombosis was the cessation of antiplatelet therapy. Figure 2. A. Occlusion of the proximal left anterior descending artery in the place of bioresorbable vascular scaffold implantation (arrow); B. Plain old balloon angioplasty performed in the occluded left anterior descending artery; C. Good final angiographic result of the treatment of scaffold thrombosis (TIMI 3) Figure 1. A. Coronary angiography revealing critical stenosis of the proximal left anterior descending artery (arrow); B. Good angiographic result of primary angioplasty with bioresorbable vascular scaffold implantation (TIMI 3); C–F. Good scaffold expansion and complete strut apposition in optical coherence tomography A

Heat Stroke–Induced Sinoatrial Node Dysfunction

BackgroundHeat stroke has been associated with stress-induced cardiomyopathy and electrocardiogram ST segment elevation and depression. Laboratory studies with dogs have demonstrated heat stroke–induced sinoatrial node dysfunction in the setting of hyperkalemia. No prior case report has described heat stroke–induced complete sinoatrial node dysfunction that resolved in the emergency department. Case ReportAn 87-year-old female presented to the emergency department with heat stroke and severe bradycardia. Initial electrocardiogram demonstrated complete sinoatrial node dysfunction. The bradycardia responded to external cardiac pacing and the sinoatrial node dysfunction resolved with aggressive cooling. Emergency physicians should be aware that heat stroke can cause complete sinoatrial node dysfunction and that this bradydysthrmia can be treated with aggressive cooling.

Severe Hyperthyroidism Presenting with Acute ST Segment Elevation Myocardial Infarction.

Introduction. Acute myocardial infarction is life-threatening. A cardiac troponin rise accompanied by typical symptoms, ST elevation or depression is diagnostic of acute myocardial infarction. Here, we report an unusual case of a female who was admitted with chest pain. However, she did not present with a typical profile of an acute myocardial infarction patient. Case Presentation. A 66-year-old Han nationality female presented with chest pain. The electrocardiogram (ECG) revealed arched ST segment elevations and troponin was elevated. However, the coronary angiography showed a normal coronary arterial system. Thyroid function tests showed that this patient had severe hyperthyroidism. Conclusion. Our case highlights the possibility that hyperthyroidism may cause a large area of myocardium injury and ECG ST segment elevation. We suggest routine thyroid function testing in patients with chest pain.

Total Flavones of Choerospondias axillaris Attenuate Cardiac Dysfunction and Myocardial Interstitial Fibrosis by Modulating NF-κB Signaling Pathway

This study aimed to investigate the effect of total flavonoids of Choerospondias axillaris (TFC) on myocardial infarction (MI)-induced cardiac dysfunction, interstitial fibrosis and inflammatory reaction and further to clarify the potential signaling pathway involved. Rats were subjected to MI via coronary artery occlusion. The model establishment was confirmed by the occurrence of ST-segment elevation in electrocardiogram. Then, TFC was administrated at doses of 75, 150 and 300 mg/kg for 28 consecutive days (gavage). Body weight and heart weight were recorded. Hemodynamics, infarct size and myocardial fibrosis were examined. Blood samples were collected to determine tumor necrosis factor-α (TNF-α) and interleukin 6, 10 (IL-6, IL-10) levels. The expressions of matrix metalloproteinases-2, 9 (MMP-2, 9), phosphor-IKBα (p-IKBα) and transforming growth factor-β1 (TGF-β1) were assayed by Western blot. The results indicated that TFC significantly improved cardiac dysfunction, the heart coefficient and myocardial fibrosis in MI rat. TFC also decreased the levels of TNF-α and IL-6, but increased IL-10 content. Moreover, treatment with TFC protected the heart from chronic MI injury by decreasing the expressions of MMP-2, 9, TGF-β1 and p-IKBα. The results suggested that TFC attenuated cardiac dysfunction and myocardial interstitial fibrosis by modulating nuclear factor-kappa B (NF-κB) signaling pathway.

Intracoronary electrocardiogram ST-segment elevation in patients with non-ST-segment elevation myocardial infarction and its association with culprit lesion location and myocardial injury

An intracoronary electrocardiogram (IC-ECG) is a sensitive method to detect local myocardial ischaemia. We investigated the prevalence of IC-ECG ST-segment elevation (STE) with respect to culprit lesion location in patients with non-ST-segment elevation myocardial infarction (NSTEMI) and its relationship with elevated levels of cardiac biomarkers. We examined 87 NSTEMI patients who underwent IC-ECG recording by locating the insulated polymer-coated guidewire distal to the culprit lesion before percutaneous coronary intervention (PCI). Cardiac biomarkers were serially examined. IC-ECG STE was observed in 24 patients (27.6%) before PCI, and was significantly more frequent in patients with LCx culprit lesions (LAD vs. LCx vs. RCA, 12.1% vs. 53.3% vs. 16.7%; p<0.001). Peak cardiac troponin I (cTnI) values were associated with IC-ECG STE, ejection fraction (EF), cTnI values on admission, and type B2/C lesions. In multivariate analysis, IC-ECG STE (odds ratio [OR], 5.04; 95% confidence intervals [CI]: 1.51-16.85; p=0.009), and EF (OR, 0.95; 95% CI: 0.90-1.00; p=0.043) were predictors of greater peak cTnI values. IC-ECG STE was not uncommon in NSTEMI patients, particularly those with LCx culprit lesions. IC-ECG monitoring before PCI may help identify NSTEMI patients with high risk of greater myocardial injury.

A diagnostic dilemma: early repolarization syndrome associated with ventricular fibrillation

An early repolarization (ER) pattern, characterized by J-point elevation, slurring of the terminal part of the QRS and ST-segment elevation, is a common finding on the 12-lead electrocardiogram. It has been suggested that J-point elevation, which was considered benign for many years, may play a critical role in the pathogenesis of idiopathic ventricular fibrillation (VF). Recent studies have shown that an ER pattern in inferior leads or inferolateral leads is associated with increased risk for life-threatening arrhythmias. We report the case of a 52-year-old man with no structural heart disease whose electrocardiogram showed type 2 ER pattern (with evidence of J-point and ST-segment elevation in electrocardiogram leads II, III, and aVF). The patient presented with VF.

Successful primary angioplasty in patient with ST-segment elevation myocardial infarction caused by large septal branch occlusion

We report a rare case of septal ST-segment elevation myocardial infarction (STEMI) caused by isolated, thrombotic occlusion of a large septal branch successfully treated with drug-eluting stent (DES) implantation. The patient was a 56-year-old male, with past medical history of stable angina for two years, arterial hypertension, and diabetes mellitus, in whom the diagnosis of septal wall STEMI was made by ambulance team at home. Patient received 300 mg of aspirin, 600 mg of clopidogrel and 5000 units of unfractionated heparin. He presented in primary-PCI center with crushing retrosternal chest pain lasting two hours. In the electrocardiogram ST-segment elevation in leads V1 to V3 was found (Fig. 1). Immediate coronary angiography of the right coronary artery using femoral approach and standard 6 French diagnostic catheter was performed showing a chronic total occlusion of the proximal right coronary artery with good collateral flow (Fig. 2A). In the angiography of the left coronary artery performed using Launcher (Medtronic Vascular, USA) 6 French Judkins left guiding catheter a chronic total occlusion of the mid left circumflex artery with retrograde filling from collaterals was demonstrated (Fig. 2B).

Ictus y síndrome de takotsubo: una relación recíproca

Takotsubo syndrome is a transient stress cardiomyopathy associated with a distinctive left ventricular contraction pattern. It has been described as a cardioembolic source or as a consequence of stroke. Two patients are reported that illustrate the reciprocal relationship between Takotsubo syndrome and stroke and the physiopathological mechanisms implicated are analyzed. Two women aged 70 and 78 years respectively are described. The first one was admitted with electro-cardiogram ST-segment elevation, slight troponin elevation and stroke symptoms. Ecocardiography and cardiac magnetic resonance findings were consistent with Takotsubo syndrome that was the probable source of cardioembolic stroke. The second patient suffered a Takotsubo syndrome 72 hours after a brain infarction involving the insular cortex that was considered the trigger of Takotsubo syndrome. Takotsubo syndrome and stroke may have a reciprocal etiological relationship that is suggested by the temporal profile between the two processes. Cardiac magnetic resonance may aid in the establishment of the diagnosis of Takotsubo syndrome.

Assessment of left ventricular twist mechanics in Tako-tsubo cardiomyopathy by two-dimensional speckle-tracking echocardiography

To assess left ventricular (LV) twist mechanics in patients with Tako-tsubo cardiomyopathy (TTC). Two-dimensional strain and LV twist by speckle-tracking echocardiography was performed in 17 consecutive patients with typical TTC according to the Mayo clinic criteria [78 ± 8 years, 88% women, and mean left ventricular ejection fraction (LVEF) 45 ± 10%], at the acute phase (within 24 h after admission) and after recovery (1 month later). Seventeen control (C) patients matched for age and sex (mean LVEF 70 ± 7%), and 17 patients with acute anterior myocardial infarction (MI) treated by successful primary angioplasty 24 h before, matched for LVEF, age, and sex, were compared with TTC patients. LV twist was assessed using the parasternal basal and apical short-axis planes, and defined as the net difference in degrees of apical (Ar) and basal rotation (Br). Peak systolic and early diastolic, apical (As and Ad) and basal (Bs and Bd) rotation rate, and LV twisting rate (TR) and untwisting rate (UR) (in °/s) were derived from rotational and twist curves. The time sequences were normalized to the percentage of systolic duration. At the acute phase, Ar, As, Ad, Bs, LV twist (10 ± 9° vs. 23 ± 6°), LV TR, and LV UR were significantly impaired in patients with TTC when compared with controls (all, P < 0.05). Patients with MI displayed intermediate values (P = NS vs. TTC, and P < 0.05 vs. C). However, in the subgroup of patients with electrocardiogram ST-segment elevation at presentation (n = 12 TTC and 17 MI), several LV twist mechanics parameters were significantly reduced in TTC patients when compared with MI patients, LV twist, and LV TR being the most significant factors (all, P≤ 0.01). Abnormal reversed Ar (clockwise when seen from the apex) was seen in three patients (18%) with TTC vs. none in the other groups. A significant correlation between LV twist and LVEF, LV volumes, wall motion score index, and plasma NT-pro BNP was observed in the TTC group (all, P < 0.05). At follow-up, LV twist mechanics improved significantly in TTC patients (all, P < 0.05 vs. acute phase), who had final values similar to C (all, P = NS), whereas the magnitude of improvement was lower in MI patients (P ≤ 0.05 vs. TTC). LV twist mechanics is significantly impaired in patients with TTC mainly due to a severe reduction in apical function and is entirely reversible. Furthermore, in the subgroup of patients with ST-segment elevation, the early post-admission evaluation of LV twist mechanics is more severely impaired in TTC when compared with MI.

Brugada syndrome and atrial fibrillation: pathophysiology and genetics

In 1992, the Brugada brothers described eight patients with a syndrome of ST segment elevation in electrocardiogram (ECG) leads V1–V3 accompanied by a right bundle branch block appearance and the risk of ventricular fibrillation and sudden cardiac death.1 One patient was an 8-year-old girl with an additional history of paroxysmal atrial fibrillation (AF). She had experienced her first paroxysm soon after birth while her first episode of syncope occurred at 8 years of age. Since this first description a dramatic variability in clinical presentation of the disease has transpired. A high prevalence of AF has, however, remained a feature.2 The first gene linked to the Brugada syndrome was SCN5A, which encodes the α-subunit of the NaV1.5 cardiac sodium channel responsible for the inward sodium current. A 20% yield of disease-associated variants has consistently been reported.2 More recently less common mutations in other genes have been associated with the Brugada syndrome including mutations in: GPD1L, involved in the transportation of cardiac sodium channels to the cell membrane; SCN1B and SCN3B, encoding β-subunits of NaV1.5; KCNE3 encoding a β-subunit of the channel responsible for the I (to) current; and CACNA1C and CACNB2b, which both encode subunits of the L-type calcium channel.3 Mutations in SCN5A have also been reported in association with familial AF.4 The prevalence of AF and atrial flutter in patients with Brugada syndrome is approximately 20%2 compared with 2.3% in the general population above the age of 40.5 Kusano et al . found that 70% of episodes of AF in their Brugada patients occurred at night, suggesting that nocturnal vagal activity and withdrawal of sympathetic activity may play an important role in arrhythmogenesis. Bradycardia …

An accordion phenomenon with ST-segment elevation of electrocardiogram and anginal chest pain: A case report

Tortuous coronary arteries frequently make percutaneous coronary intervention (PCI) difficult by causing less accessibility of guidewire toward the target lesion. After guidewire has been passed through the target lesion, it often assists a balloon catheter and stent system insertion along the stiff guidewire. However, artificial kinking and wrinkling might induce pseudo-narrowing of coronary arteries, which has been recognized as an “accordion phenomenon.” We describe an educational case of an accordion phenomenon with ST-segment elevation of electrocardiogram and anginal chest pain when the stiff guidewire which had been withdrawn was advanced again into the distal site after deploying stents.

Exercise-induced ventricular tachycardia associated with J point ST-segment elevation in inferior leads in a patient without apparent heart disease: a variant form of Brugada syndrome?

Exercise-induced monomorphic ventricular tachycardia originating in the right ventricular outflow tract without evidence of structural heart disease can be idiopathic or can be the harbinger of structural abnormalities such as arrhythmogenic right ventricular dysplasia. Recently, the so-called variant Brugada syndrome has been reported in very few cases in the literature and is much less electrophysiologically defined in terms of its clinical significance. We present the case of a 21-year-old man with exercise-induced monomorphic ventricular tachycardia (left bundle-branch block/right axis deviation), without detectable structural heart disease, with evidence of J point and ST-segment elevation in electrocardiogram leads II, III, and aVF after intravenous administration of propafenone. This is followed by a brief discussion on the new concept of “variant Brugada syndrome,” drug-induced electrocardiographic changes, normal-variant repolarization abnormality, and idiopathic right ventricular outflow tract tachycardia.

ST-segment Elevation of Electrocardiogram in a Patient with Shoshin Beriberi

We report a case of a 58-year-old man with Shoshin beriberi who demonstrated ST-segment elevation and myocardial damage without coronary artery stenosis. The patient subsequently recovered with thiamine treatment. We conclude that it is important to consider Shoshin beriberi as part of the differential diagnosis in patients with shock and ST-segment elevation.

The influence of fish oil diet and norepinephrine treatment on fatty acid composition of rat heart phospholipids and the positional fatty acid distribution in phosphatidylethanolamine.

The effect of chronic norepinephrine (NE) administration with increasing dosage from 1-4 mg/kg over a period of 2 weeks was studied on cardiac phospholipids and their fatty acid distribution in rats. Animals were fed a control diet or a 10% cod liver oil (CLO)-enriched diet. The relative distribution of various polyunsaturated fatty acids esterified to the 1- and 2-position of the phosphatidylethanolamine fraction was estimated. NE stress during control feeding significantly reduced the total phospholipid content in rat heart. No differences in the phospholipid class distribution were found. However, CLO feeding as well as chronic NE administration resulted in a decrease of omega 6 fatty acids, mainly C 18:2 omega 6 and C 20:4 omega 6, which was compensated with an increase in omega 3 fatty acids, mainly C 20:5 omega 3 and C 22:6 omega 3. The changes in fatty acid composition qualitatively agree with those reported by Gudbjarnason et al. (23), except that the mortality in our NE-treated control or CLO-fed groups was considerably lower. It can probably be attributed to a different mode of NE administration. On the other hand, at the end of the CLO feeding period in rats treated with NE or not, comparing with control fed rats without NE treatment, the incidence rate of ST segment elevation in electrocardiogram (ECG) recorded under light diethylether-induced anesthesia was higher. Independent of whether the fatty acid composition of myocardial phospholipids was dietary or pharmacologically manipulated, most of the polyunsaturated fatty acids were found at the 2-position of the phosphatidylethanolamine molecules. The polyunsaturated fatty acids account for 45-50% of the fatty acyl residues and preferentially occupy the 2-position, where they can exchange for each other.

Precordial and epicardial surface potentials during Myocardial ischemia in the pig. A theoretical and experimental analysis of the TQ and ST segments.

The solid angle theorem was used to analyze the relationships between TQ and ST segment deflections recorded from precordial and epicardial locations and the time course, size, shape, and transmural location of the ischemic process in the ventricular myocardium. Mathematical predictions were compared with experimental data from the intact heart. Precordial electrograms obtained in anesthetized close-chest pigs were compared with epicardial electrograms recorded directly from the heart's surface. Various areas of ischemia were produced by occluding large and small coronary artery branches, and the resultant changes in ischemic shape were delineated with Thioflavin S injections and postmortem ultraviolet photography. Formally derived equations and cumulative experimental data were in close agreement, suggesting that in the ischemic ventricle (1) TQ depression always accompanies ST elevation, (2) TQ and ST segment changes in magnitude and polarity are complex functions of ischemic size, shape, and transmural location; (3) precordial electrocardiogram (ECG) ST segment elevation is directly related to ischemic size; and (4) epicardial ECG ST segment elevation is inversely related to ischemic size. It is thus concluded that precordial and epicardial ECG TQ and ST segment deflections are complex functions of ischemic geometry and that their accurate interpretation with respect to ischemic size and shape and in the presence of pharmacological interventions is often difficult and may be misleading.