Precordial ST Elevation Research Articles

Brugada syndrome and reduced right ventricular outflow tract conduction reserve: a final common pathway?

Brugada syndrome (BrS) was first described as a primary electrical disorder predisposing to the risk of sudden cardiac death and characterized by right precordial lead ST elevation. Early description of right ventricular structural abnormalities and of right ventricular outflow tract (RVOT) conduction delay in BrS patients set the stage for the current controversy over the pathophysiology underlying the syndrome: channelopathy or cardiomyopathy; repolarization or depolarization. This review examines the current understanding of the BrS substrate, its genetic and non-genetic basis, theories of pathophysiology, and the clinical implications thereof. We propose that the final common pathway for BrS could be viewed as a disease of 'reduced RVOT conduction reserve'.

ECG FEATURES OF TAKOTSUBO CARDIOMYOPATHY IN PAKISTANI PATIENTS

Objectives: Takotsubo cardiomyopathy (TC) is a distinct clinical disease that mimics the clinical and ECG features of ST elevation Myocardial Infarction (STEMI). Differentiating between TC and STEMI is essential since they have different treatment strategies and prognosis, especially in the acute phase. Since ECG is the first investigation for a patient with clinical features of STEMI, recognizing ECG features of TC early on is invaluable. There is a dearth of literature from the South Asian population describing ECG features of TC. Hence we investigated the different ECG features of TC in comparison to ECG features of anterior STEMI in a cohort of Pakistani population. Methodology: A retrospective analysis of first presentation ECG’s of 32 TC patients admitted in AKUH from January 2010 to December 2019 was done. TC was diagnosed using the Mayo clinic diagnostic criteria. Major exclusion criteria were patients with ECG features of left or right bundle branch block and left ventricular hypertrophy were excluded. Similar number of acute anterior STEMI patients (coronary angiogram proven) was identified and first presentation ECG features evaluated. 6 different ECG criteria to differentiate between TC and acute anterior STEMI were examined for diagnostic accuracy. Results: Patients with TC were younger and 81% of the patients were females .50% of the TC patients had precordial ST elevation >1.5mm. Reciprocal ECG changes were significantly lesser in the TC patients. The QTc interval was prolonged (>440msec) in 62.5% of the TC patients (20 patients) with a mean QTc of 456 +/- 48 msec. Q waves was seen lesser in TC patients (15.6 % vs 43.4%). All the ECG criteria examined for diagnostic accuracy for differentiating between TC and anterior STEMI had low sensitivity and high specificity. The highest sensitivity was 66 % for the criteria STe V2<1.75 mm and STe V3<2.5 mm in our population. Conclusion: This study demonstrates that published ECG criteria to distinguish TC from acute, anterior STEMI in Pakistani patients have a low diagnostic accuracy. Our study also shows that ECG of TC patients have lesser reciprocal ECG changes & Q waves, and longer QTc intervals. Novel ECG criteria amalgamating these findings can be developed to improve the accuracy of ECG diagnosis of TC. Keywords: Takotsubo Cardiomyopathy, Stress Cardiomyopathy, Electrocardiography, Cardiology

Acute myocardial infarction caused by left anterior descending artery occlusion presenting as inferior ST elevation and anterior ST depression

We report a case of acute myocardial infarction caused by left anterior descending artery occlusion presenting as ST elevation in the inferior leads and ST depression in the precordial leads, suggesting an involvement of the right coronary artery (RCA). However, coronary angiography (CAG) showed a complete occlusion of the proximal left anterior descending (LAD) coronary artery and collaterals from the left circumflex coronary artery and the RCA. Although he underwent primary percutaneous coronary intervention (PCI), he had chest pain at four days after primary PCI. His electrocardiogram (ECG) showed precordial ST elevation, suggesting an involvement of the LAD. Emergent CAG showed a complete occlusion of the proximal LAD without collaterals, but his ECG showed precordial ST elevation that was different from ST changes seen on admission. These unusual ST-segment changes might be associated with a weaker anterior ischemia due to collaterals and a strong inferior ischemia due to wrapped LAD artery.<Learning objective: Inferior ST elevation and anterior ST depression generally indicate inferior myocardial infarction. However, the unusual ST-segment changes seen in this patient with anterior myocardial infarction might be associated with a weaker anterior ischemia due to collaterals and a strong inferior ischemia due to wrapped left anterior descending artery.>

第7回 心臓性急死研究会 5年間経過観察できたST上昇を伴う徐脈依存性特発性心室細動の1症例:過換気負荷試験による検討

第7回 心臓性急死研究会 5年間経過観察できたST上昇を伴う徐脈依存性特発性心室細動の1症例:過換気負荷試験による検討

Dynamics of electrocardiographic changes, brain-natriuretic peptide and cortisol levels in a patient with stress (takotsubo) cardiomyopathy: A case report

Takotsubo cardiomyopathy is a transient acute heart failure syndrome caused by stress that provokes left ventricular mid-apical akinesis and mimics acute coronary syndrome. A 66-year-old woman had chest pain and dispnoea a few hours before hospitalization. A sudden emotional stressful event preceded the symptoms. Electrocardiographic abnormalities--precordial ST elevation and modest increase of cardiac troponin mimiced acute myocardial infarction. However, echocardiographic examination showed apical ballooning with markedly diminished left ventricle ejection fraction and the obstruction in the outflow tract of the left ventricle. Coronary angiography at admission showed no coronary stenosis and slower blood flow through the left anterior descending artery. According to anamnesis, echocardiography and coronarography finding we established the diagnosis of stress cardiomyopathy--takotsubo cardiomyopathy. We described in details the slow but dynamic electrocardiographic changes, levels of brain natriuretic peptide, cortisol and echocardiography evolution of disease during a 4-month follow-up till the full recovery. Stress (takotsubo) cardiomyopathy--became an important differential diagnosis of acute anterior myocardial infarction and it should be reconsidered every time when emotionally stressed patients with transient-apical akinesis or dyskinesis of the LV are present.

Syncope and ST Elevation in Precordial Leads

Syncope and ST Elevation in Precordial Leads

Loss-of-Function Sodium Channel Mutations in Infancy

The role of channelopathies in the pathogenesis of sudden cardiac death in patients with structurally normal hearts is a rapidly evolving story.1 Many ion channels are involved, including loss-of-function sodium channelopathies, of which the phenotypic spectrum ranges from lethal arrhythmias to asymptomatic carriers and includes Brugada syndrome (BrS), cardiac conduction disease, sick sinus syndrome, atrial fibrillation, and dilated cardiomyopathy. BrS, characterized by right precordial ST elevation on the ECG, is frequently associated with conduction delay, potentially lethal arrhythmias, and a positive family history of sudden premature death. BrS is estimated to be responsible for ≈4% of all sudden deaths and 20% of sudden deaths in patients with structurally normal hearts. Despite an overall prevalence of ≈5/10 000 individuals,2 BrS is considered extremely rare in the pediatric population. However, children harboring loss-of-function mutations in the gene coding for the sodium channel α-subunit ( SCN5A ) have been reported to present with life-threatening arrhythmias, especially during febrile episodes.3 While SCN5A mutations account for 11% to 28% of BrS probands, mutations of the L-type calcium channel, including the gene coding for the L-type calcium channel β-subunit ( CaCNB2 ), among others, have recently been implicated in ≈13% of patients with BrS-related phenotypes and sudden cardiac death.4 Article see p 14 In this issue of Circulation , Kanter et al5 describe their experience with very young children manifesting ventricular arrhythmias due to previously undetected loss-of-function sodium and/or calcium channelopathies. Twenty of 32 patients <2 years of age with rapid ventricular tachycardia (VT) or ventricular fibrillation (VF), had known structural heart disease, and 9 of the remaining 12 patients had intraventricular conduction delay (IVCD) or Brugada pattern (coved) ECG, of which 4 had associated conditions (myocarditis, Barth syndrome, and drug use). The clinical features and subsequent management and follow-up of the remaining 5 patients …

Bidirectional Precordial ST Changes during Angioplasty to Right Coronary Artery

Emergency coronary angiography of a 53-year-old man with acute coronary syndrome revealed stenosis in right coronary artery. During angioplasty, the ECG change showed three kind of ST deviation, namely inferior ST elevation with precordial ST depression, inferior ST elevation with precordial ST elevation, and inferior ST depression with precordial ST elevation. The present case shows that the ST deviation of the inferior ischemia with right ventricular ischemia takes various patterns. This phenomenon is decided by degree of right main coronary and right side branch blood flow.

Acute Myocardial Infarction by Right Coronary Artery Occlusion Presenting as Precordial ST Elevation on Electrocardiography

It is rare to observe ST-segment elevation in only the anterior leads and not the inferior leads during right coronary artery occlusion. We describe a case with acute myocardial infarction (MI) by right coronary artery occlusion who developed ST-segment elevation only in the precordial leads V1 to V3.

Clinical Predictors of Incomplete ST-Segment Resolution in the Patients With Acute ST Segment Elevation Myocardial Infarction

Background and ObjectivesThe failure of ST-segment resolution (STR) after primary percutaneous coronary intervention (pPCI) is associated with adverse clinical outcomes. However, the clinical predictors on admission for incomplete STR are poorly known.Subjects and MethodsPatients undergoing pPCI (n=101, 79 males and 22 females, mean age 60.0 years) were divided into complete STR group (≥70%, n=58) and incomplete STR group (<70%, n=43). The groups were compared according to clinical factors including history, electrocardiographic (ECG) patterns, angiographic features and laboratory data.ResultsThe incomplete STR group contained more frequent hypertensive patients (p=0.04) and patients displaying longer tendency in total chest pain duration (p=0.08). This group was associated with worse clinical factors such as low ejection fraction (p=0.06), higher Killip class (p=0.08) and more death (p=0.042). Grade 3 ischemia pattern of ECG and precordial ST elevation (i,e anterior myocardial infarction) at admission were more frequent in the incomplete STR group (p=0.001 and 0.002, respectively). Initial troponin I, creatinin kinase -MB and brain natriuretic peptide levels were higher in the incomplete STR group (p=0.001, 0.002, and 0.043, respectively). Coronary angiography showed that culprit lesions were more frequent in left anterior descending artery than other arteries in the incomplete STR group of patients (p=0.002). Thrombolysis In Myocardial Infarction (TIMI) flow grades 2 or less before PCI was more frequent in the incomplete STR group (p=0.029). However, TIMI flow grade after PCI was not appreciably different between the two groups. Logistic regression analysis demonstrated that TIMI flow grade 2 or less was most powerful predictor for incomplete STR {odds ratio (OR)=12.12, 95% confidence interval (CI) 1.23-119.35, p=0.032}. Other independent predictors were anterior infarction (OR=3.39, CI 1.46-10.57, p=0.007), ischemia grade 3 ECG at admission (OR=3.87, CI 1.31-11.41, p=0.014), and hypertensive patients (OR=3.03, CI 1.13-8.15, p=0.027).ConclusionIncomplete STR after pPCI is associated with poor prognostic clinical factors. TIMI flow grade 2 or less before pPCI, ST elevation on precordial leads, ischemia grade 3 pattern of initial ECG, and hypertensive patients are independent predictors for incomplete STR in the early stage.

Sudden Death Prevention With Implantable Devices

The “modern” era of the treatment of ventricular tachyarrhythmias with device-based therapy may have begun in 1899, when Prevost and Battelli noted, almost as an afterthought, that direct current shock could terminate ventricular fibrillation (VF) in dogs.1 Three decades later, pioneering work in the field of defibrillation concluded that the passage of electrical current across the heart can both initiate and terminate VF.2,3 Still, little attention was paid to this phenomenon, as evidenced by Paul Dudley White’s Heart Disease , which devoted less than half a page to VF and characterized the arrhythmia as “a condition of little importance so far as we know now.”4 In 1947, the thoracic surgeon Claude Beck saved the first human life by the successful use of cardiac defibrillation in a 14-year-old boy who developed VF during a thoracic surgical procedure and went on to achieve a full recovery.5 These early accomplishments provided the foundation for the landmark work of Mirowski and Mower that ultimately led to the development of the implantable cardioverter-defibrillator (ICD) and its introduction in humans in 1980.6 Pacing may prevent sudden cardiac death due to bradyarrhythmias and in certain circumstances such as torsade de pointes associated with congenital long-QT syndrome (LQTS) and pause-dependent ventricular tachycardia (VT). Although no controlled studies exist, retrospective analyses suggest that recurrent torsade de pointes in patients with LQTS may be prevented by continuous pacing.7 Early clinical data on small numbers of patients suggested that the combination of β-adrenergic blockade plus continuous pacing reduced the number of syncopal events and the anticipated rate of sudden death in high-risk LQTS patients.8 The beneficial effects of pacing may be limited to patients with LQT2 and LQT3, in which the transmural dispersion of repolarization worsens steeply during bradycardia.9 Genotype-phenotype correlation confirms that …

Overlap Syndrome of Cardiac Sodium Channel Disease in Mice Carrying the Equivalent Mutation of Human SCN5A -1795insD

Patients carrying the cardiac sodium channel (SCN5A) mutation 1795insD show sudden nocturnal death and signs of multiple arrhythmia syndromes including bradycardia, conduction delay, QT prolongation, and right precordial ST-elevation. We investigated the electrophysiological characteristics of a transgenic model of the murine equivalent mutation 1798insD. On 24-hour continuous telemetry and surface ECG recordings, Scn5a(1798insD/+) heterozygous mice showed significantly lower heart rates, more bradycardic episodes (pauses > or = 500 ms), and increased PQ interval, QRS duration, and QTc interval compared with wild-type mice. The sodium channel blocker flecainide induced marked sinus bradycardia and/or sinus arrest in the majority of Scn5a(1798insD/+) mice, but not in wild-type mice. Epicardial mapping using a multielectrode grid on excised, Langendorff-perfused hearts showed preferential conduction slowing in the right ventricle of Scn5a(1798insD/+) hearts. On whole-cell patch-clamp analysis, ventricular myocytes isolated from Scn5a(1798insD/+) hearts displayed action potential prolongation, a 39% reduction in peak sodium current density and a similar reduction in action potential upstroke velocity. Scn5a(1798insD/+) myocytes displayed a slower time course of sodium current decay without significant differences in voltage-dependence of activation and steady-state inactivation, slow inactivation, or recovery from inactivation. Furthermore, Scn5a(1798insD/+) myocytes showed a larger tetrodotoxin-sensitive persistent inward current compared with wild-type myocytes. Mice carrying the murine equivalent of the SCN5A-1795insD mutation display bradycardia, right ventricular conduction slowing, and QT prolongation, similar to the human phenotype. These results demonstrate that the presence of a single SCN5A mutation is indeed sufficient to cause an overlap syndrome of cardiac sodium channel disease.

Transient precordial ST elevation by a spasm of the conus artery during right coronary angiography

During coronary angiography of right coronary artery (RCA), a catheter wedged into a conus artery, and a remarkable coved-type ST elevation was seen in precordial lead through V1–3. LCA angiography did not show any abnormal findings, but we recognized a slow contrast flow in a conus artery by RCA angiography. The patient was free from chest pain, and a ST elevation was improved. The slow flow of a conus artery was recovered within five minutes. Precordial ST elevation may be caused by a catheter-induced spasm of a conus artery.

Ten years of genes in inherited arrhythmia syndromes: an example of what we have learned from patients, electrocardiograms, and computers

In the last 10 years the molecular substrate of a diversity of primary electrical diseases has been unraveled. Disease-causing mutations in ion-channel genes have been identified and have challenged clinical and basic electrophysiologists to mechanistically link the observed genetic aberrancies to the phenotype. Indeed, in collaborative efforts of clinical cardiologists, clinical and molecular geneticists, basic electrophysiologists and computer modellers, the pathophysiology of many clinical electrocardiographic findings have been elucidated in detail. The family described concerns an 8-generation SCN5a-linked family with a high incidence of nocturnal sudden death. The phenotype is characterised by bradycardia-dependent QT-prolongation, right precordial ST-elevation, conduction disease at all cardiac compartments, and sinus node disfunction. Heterologous expression of the mutant sodium channels demostrated altered channel characteristics which, introduced in elegant computer modeling studies, nicely explained the complex phenotype. As such these studies serve as a good example of what can be reached in a multidisciplinary approach with clinical and basic scientists.

Brugada-Like ECG Findings Detected After Resection of Esophageal Cancer

We have observed 3 cases of Brugada like ECG findings after the resection of esophageal cancer. Case 1. A 63 years-old male who had atrial fibrillation (AF) was diagnosed as affected byesophageal cancer and underwent the resection of esophagus with subsequent reconstruction using stomach into retro-sternum. Post-operative ECG showed coved type ST elevation in lead V1-4. This finally gradually reverted in ten days after operation and normalized within 2 weeks. Case 2. A 69 year-old male, who had paroxysmal AF and esophageal cancer, received the same procedure as in case 1. His ECG revealed abnormal ST elevation in V1. In thoracic CT image, right ventricle (RV) was compressed by the reconstructed stomach. Case 3. A 68 year-old male underwent the same operation as described above. His post-operative ECG showed Brugada like ST elevation in V1-3. This ST change disappeared within 3 weeks. In none of these 3 cases, there was a family history of sudden death or syncope, and the previous ECG showed no ST segment elevation. The compression of the RV by lifted stomach was considered to induce the precordial ST elevation mimicking Brugada syndrome.

Mechanisms of syncopes in arrhythmogenic right ventricular dysplasia–cardiomyopathy beyond monomorphic ventricular tachycardia

Syncopes appear in 10–20% in arrhythmogenic right ventricular dysplasia–cardiomyopathy (ARVD/C). In the majority of cases sustained or non-sustained monomorphic ventricular tachycardias represent the underlying mechanism of syncope. In other cases the mechanism remains unclear. In 37 patients (23 females, mean age 43.6 ± 12.8 years) without detectable and inducible monomorphic ventricular tachycardia, a diagnostic algorithm including repeat ECG, holter monitoring, telemetry, electrophysiological examination, ajmaline challenge, tilt table testing and neurological work-up (EEG, cranial computer tomography) was used in order to identify the mechanism of syncopes. Constant AV block 3° could be found in 3 patients (2 males). Intermittant AV block 2° or 3° could be identified in 3 females. Four males had abnormal Wenckebach point during rapid atrial stimulation, 3 males demonstrate isolated HV interval prolongation. Rapid polymorphic VT and VF could be induced in a young female with ARVD/C. Eight patients (7 females) presented with recurrent syncopes and provocable right precordial ST elevation and right bundle branch block during ajmaline challenge. Three patients had abnormal tilt table testing as the only pathological finding. In one female with intermittent AV block 2° tilt table testing and ajmaline challenge was positive. One female had the diagnosis of focal epilepsia after neurological work-up. In 11 cases the mechanism of syncopes remained unclear. In patients with ARVD/C and syncopes beyond detectable or inducible monomorphic VT, several mechanisms of syncopes could be identified with conduction disease as the predominant finding. These results may help in identifying rare mechanisms of syncopes in ARVD/C.

Chest pain and ST elevation associated with fever in patients with asymptomatic Brugada syndrome: Fever and chest pain in Brugada syndrome

Brugada syndrome is a disease with a high risk of sudden cardiac death. Genetic mutations of the cardiac sodium channel are linked to the characteristic electrocardiogram abnormality of Brugada syndrome. Dysfunction of the mutated sodium channel is reported to be temperature-sensitive. We experienced two patients with asymptomatic Brugada syndrome who showed significant ST elevation in precordial leads while they were in a febrile state. Moreover, these patients had chest pain during precordial ST elevation. From these cases, asymptomatic Brugada syndrome should be considered as one of differential diagnoses when we examine the patients who complained of fever and chest pain. Furthermore, we should lower the elevated body temperature in patients with Brugada syndrome, because fever caused spontaneous ST elevation leading to fatal ventricular arrhythmias.

Electrophysiologic investigation in Brugada syndrome; yield of programmed ventricular stimulation at two ventricular sites with up to three premature beats.

Numerous reports on the inducibility of ventricular tachyarrhythmias (VT) in patients with atypical right bundle branch block and right precordial ST-elevation (Brugada syndrome) are based on multicentre studies that have used different stimulation protocols. Therefore, we prospectively investigated the inducibility of VT in these patients using a uniform protocol. In 41 consecutive patients (29 males) showing a pattern of right bundle branch block and ST-elevation, programmed ventricular stimulation was performed in the right ventricular apex with up to three premature stimuli at sinus rhythm and at four different paced cycle lengths (500, 430, 370, and 330 ms) until refractoriness was reached or reproducible induction of a sustained (>30s) VT occurred. If a VT was not reproducibly inducible, the same protocol was repeated in the right ventricular outflow tract. A history of life-threatening events defined as syncope (n=17) or aborted sudden cardiac death (n=13) was present in 30 patients (73%); 11 individuals were asymptomatic. Inducibility (68%) was similar between symptomatic (n=21, 70%) and asymptomatic patients (n=7, 64%). In 16 (39%) patients, VT were reproducibly inducible. If patients were only stimulated in the right ventricular apex, inducibility rate decreased to 39%. If only two premature beats at two sites were used it was as low as 32%. The mean coupling intervals of the second and third premature stimuli inducing sustained VT were short: 189+/-21 ms vs 186+/-22 ms, respectively. Forty-four percent of all patients (i.e. 64% of the inducible patients) had inducible VT only with coupling intervals shorter than 200 ms. The stimulation protocol markedly influences the extent of inducibility of VT in patients with right bundle branch block and ST-segment elevation. These findings question the significance of previous multicentre studies using different stimulation protocols and should have implications for further studies.

Women with acute anterior myocardial infarction have less precordial ST elevation than men independent of age of presentation R.S. Wright, Wayne L. Miller, Ihor Gussak, David L. Dvorak, Thomas P. Aufdenheide, John H. Haley, Stephen L. Kopecky, Guy S. Reeder, Stephen C. Hammill. Mayo Clinic, Rochester, MN

Women with acute anterior myocardial infarction have less precordial ST elevation than men independent of age of presentation R.S. Wright, Wayne L. Miller, Ihor Gussak, David L. Dvorak, Thomas P. Aufdenheide, John H. Haley, Stephen L. Kopecky, Guy S. Reeder, Stephen C. Hammill. Mayo Clinic, Rochester, MN

Risk stratification of sudden cardiac death and malignant ventricular arrhythmias in right ventricular dysplasia-cardiomyopathy

Arrhythmogenic right ventricular dysplasia-cardiomyopathy is in most cases a benign cause of ventricular arrhythmias in young patients. The major reason of mortality is sudden arrhythmic death with an annual rate of 2–3% as the first manifestation of the disease in most cases. Little is known about risk factors of sudden arrhythmic death so far. The purpose of the retrospective study was to classify risk factors from invasive and non-invasive examinations. Methods: In a cohort of 121 consecutive patients sampled from 1986 to 1998 the value of right ventricular dilatation, left ventricular involvement analysed by angiocardiography or echocardiography and standard ECG parameters such as precordial T wave inversions, right precordial ST elevation, precordial QRS dispersion, left precordial JT interval prolongation and complete right bundle branch block were determined. The whole cohort of patients were divided into two groups with high arrhythmic risk (aborted or non-aborted sudden death, recurrent ventricular tachycardia despite medical treatment, recurrent syncopes) and low risk (frequent ventricular premature beats, non sustained ventricular tachycardia, uneventful course under medical therapy). Results: From angiocardiography or echocardiography in a quantitative approach right ventricular dilatation ( p<0.0001) and additional left ventricular abnormalities ( p<0.0001) could be identified as major risk factors. From an ECG point of view increased precordial QRS dispersion ≥50 ms ( p<0.01) with complete right bundle branch block and right ventricular dilatation in most cases and precordial T wave inversions beyond V3 ( p<0.0001) and the phenomenon of left precordial JT interval prolongation (JT dispersion ≥30 ms) in cases of additional left ventricular abnormalities represented non-invasive predictors of recurrent arrhythmic events. Right precordial ST segment elevation could be excluded as risk factor of sudden arrhythmic death. Conclusions: Right ventricular dilatation with ECG depolarisation abnormalities and additional left ventricular involvement with striking ECG repolarisation abnormalities could be identified as strong risk factors of recurrent arrhythmic events in ARVD with unfavorable prognosis.