Telltale termination of an A-on-V tachycardia with two blocked atrial activations: What is the mechanism?

The termination of tachycardia may provide important clues toward the mechanism of the tachycardia and that close vigilance may clinch the diagnosis before proceeding to other pacing maneuvers.

An Incessant Tachycardia with Alternating QRS Complexes: What Is the Mechanism?

We present a patient with ischemic cardiomyopathy who had ventricular tachycardia (VT) with QRS morphology alternans. The electrophysiological findings, in this case, supported the occurrence of antegrade activation of the proximal His-Purkinje system during VT, with the ultimate electrocardiogram morphology dependent on fusion from intramyocardial and His-Purkinje activations.

An Unusual Electrogram Sequence with a Questionable Potential on the His-bundle Catheter During Sinus Rhythm: What Is the Mechanism?

The presence of 2 ventricular signals caused by structures near the His bundle region is rare. Some associative and dissociative maneuvers for dissociating a certain electrical signal from others of known origin are used to ascertain the source of an unknown potential.

Accessory Pathway in Ebstein's Anomaly: Absence of Evidence Is Not Evidence of Absence.

Electrocardiography has certainly great merit and is almost abnormal in most patients with Ebstein's anomaly. Incomplete or complete right bundle brunch block (RBBB) is seen in almost half of these patients. The absence of the expected RBBB during sinus rhythm in a patient with Ebstein's anomaly is a useful clue of pre-excitation in these patients.

Relation Between Globulin, Fibrinogen, and Albumin With the Presence and Severity of Coronary Artery Disease.

The albumin to globulin ratio (AGR) is used as a prognostic marker in acute ischemic cardiovascular events. We investigated whether serum AGR, fibrinogen, and fibrinogen to albumin ratio (FAR) are related to the presence and severity of coronary artery disease (CAD). Patients who underwent coronary angiography procedures were analyzed retrospectively. The severity of CAD was assessed by the Gensini score. The study population (3031 patients; 1071 females and 1960 males) was divided into 3 tertiles based on AGR values. Gensini score, lipid levels, diabetes mellitus (DM), hypertension (HT), age, and fibrinogen level were higher in the low AGR group. Pearson correlation analysis showed that AGR (r = -0.068, P < .001) was negatively and fibrinogen (r = 0.187, P < .001) was positively correlated with the Gensini score. Male gender, HT, smoking, DM, age, high triglyceride (TG) level, low-density lipoprotein cholesterol (LDL-C) >160 mg/dL, estimated glomerular filtration rate (eGFR) <60 mL/min, and fibrinogen level >3.5 g/L were independent predictors of CAD. Male gender, age, eGFR, DM, LDL-C, TG, and FAR had an independent positive relation to the Gensini score. In conclusion, similar to traditional risk factors, plasma fibrinogen and albumin levels showed a close relation with the presence and severity of CAD.

A Wide QRS Tachycardia with Three Distinct Left Bundle Branch Block Morphologies in a Patient with Sinus Rhythm with Left Bundle Branch Block: What Is the Mechanism?

The differential diagnosis for a wide complex tachycardia includes all causes of supraventricular tachycardia (SVT) with bundle branch block or all causes of SVT with antegrade pre-excitation by bystander involvement of any accessory pathways, myocardial or bundle brunch ventricular tachycardia, and antidromic (atriofascicular or nodofascicular/nodoventricular) and other pre-excited reciprocating tachycardias. We present a case of wide complex QRS tachycardia with a left bundle branch block QRS morphology.

The transition of the tachycardia from narrow to wide by a spontaneous atrial premature beat: What is the mechanism?

The transition of the tachycardia from narrow to wide by a spontaneous atrial premature contraction causing a long-short sequence and right bundle branch block.

A dual nodal response to the parahisian pacing and induction of the retrograde right bundle branch block maneuvers.

We presented intracardiac electrograms during the parahisian pacing, which represent three types of retrograde conduction and focus on the mechanism of types of retrograde conduction on wide QRS complexes and conclude that the two types of QRS of the retrograde conduction resulted from the presence or absence of retrograde block at the right bundle branch.

Circulating CD4+CD25+ T cells in rheumatic mitral stenosis.

BACKGROUND AND AIM OF THE STUDY: Autoimmunity plays an essential role in the pathogenesis of rheumatic heart disease. Although the ongoing rheumatic process has been demonstrated with high levels of inflammatory markers, the cellular mechanism(s) of autoimmunity have not yet been investigated. The study aim was to examine levels of circulating CD4+CD25+ T cells in patients with rheumatic mitral stenosis, and to evaluate the relationship between regulatory CD4+CD25+ T-cell count and clinical and echocardiographic measures. METHODS: A total of 42 patients with mitral stenosis was enrolled into the study, and 27 normal age- and gender-matched healthy subjects served as controls. All patients and controls underwent clinical, electrocardiographic, echocardiographic and laboratory evaluation. T-cell levels were determined with flow cytometry using monoclonal fluorescein isothiocyanate-labeled anti-CD4 and phycoerythrin-labeled anti-CD25 antibodies. RESULTS: The circulating CD4+CD25+ T-cell count was significantly lower in patients with mitral stenosis than in controls (231 +/- 120 versus 372 +/- 180 per mm3; p = 0.001). The percentage ratio of CD4+CD25+ T cells to total leukocytes and lymphocytes was significantly lower in patients with mitral stenosis than in controls (2.9 +/- 1.5 versus 5.2 +/- 2.1; p < 0.001, and 11.2 +/- 5.6 versus 14.8 +/- 5.6; p = 0.011, respectively). In addition, a significant negative correlation was identified between the erythrocyte sedimentation rate and circulating CD4+CD25+ T-cell count (Spearman rho = -0.414; p = 0.006). No correlation was found between CD4+CD25+ T-cell count and clinical and echocardiographic parameters in patients with mitral stenosis. CONCLUSION: A decrease in CD4+CD25+ T cell numbers in mitral stenosis patients might suggest a role for cellular autoimmunity in a smoldering rheumatic process.

Comparison of the electrocardiographic features of complete left bundle branch block in patients with ischemic and nonischemic left ventricular dysfunction.

BACKGROUND: Differentiating ischemic (ILVD) from nonischemic left ventricular dysfunction (NILVD) is important prognostically and therapeutically but might be difficult clinically. The differentiating role of electrocardiographic (ECG) features in the presence of left bundle-branch block (LBBB) is debatable on differentiating ILVD from NILVD. OBJECTIVE: The present study assessed whether there is the role of certain ECG features in differentiating ILVD from NILVD in the presence of the complete LBBB. METHODS AND RESULTS: Patients who had LBBB were divided into two groups based on the presence and type of left ventricular dysfunction; (1) ILVD group (49 patients; 20 female; age: 65 +/- 11 years) and (2) NILVD group (49 patients; 22 female; age: 59 +/- 12 years), and numerous ECG features were compared. Most of these ECG features did not show any difference between the groups except for following ECG findings; the voltage of R wave in V6 were statistically higher in NILVD group compared ILVD group (p: 0.03); the depression of the ST-J point by more than 0.2 mV in V6 were also frequently observed in NILVD group compared ILVD group (5/ 10% vs 19/ 39% , p: 0.001); and the notching in the ascending or descending limb of the S wave in V1-4 leads were more in ILVD group (18/ 36% vs 8/ 16% p: 0.03; 9/ 16% vs 2/ 4%, p: 0.03, respectively). CONCLUSION: In the current study, although some ECG findings were found to be useful, ECG features in the presence of complete LBBB had poor value in differentiating ILVD from NILVD.

Comparison of presence and extent of coronary narrowing in patients with left bundle branch block without diabetes mellitus to patients with and without left bundle branch block but with diabetes mellitus.

We prospectively analyzed the clinical, echocardiographic, and coronary arteriographic data of 51 patients with type 2 diabetes mellitus with left bundle branch block (LBBB), 51 patients with type 2 diabetes mellitus without LBBB, and 51 patients with isolated LBBB matched for age and gender. Extent of coronary artery disease (CAD) was classified according to the standard method into 1-, 2-, or 3-vessel disease and was estimated by calculation of the Gensini score. The left ventricular ejection fraction was analyzed by echocardiography. Age, gender, and percentage of patients with a smoking habit or family history of CAD did not differ among the groups. The rates of hypertension and levels of serum creatinine, cholesterol, and triglycerides were statistically higher in group I compared with the other 2 groups. Patients with diabetes and LBBB (group I) had significantly higher scores for the severity (Gensini score) of CAD (p <0.001) and more 3-vessel disease (p <0.001). After adjustment for hypertension, hypertriglyceridemia, and hypercholesterolemia with covariance analysis, the presence of LBBB was also associated with a higher Gensini score in patients with diabetes compared with those with diabetes but without LBBB and those with isolated LBBB (p <0.001). The present study, for the first time, has shown that patients with type 2 diabetes mellitus and concomitant LBBB have more severe and extensive CAD and advanced left ventricular dysfunction compared with those with diabetes but without LBBB and those with isolated LBBB.

Clinical features of isolated ventricular noncompaction in adults long-term clinical course, echocardiographic properties, and predictors of left ventricular failure.

BACKGROUND: Isolated ventricular non-compaction (IVNC) is a rare disorder characterized by prominent trabecular meshwork and deep recesses. We retrospectively assessed the clinical characteristics and natural course of IVNC in adults diagnosed at our hospital. METHODS AND RESULTS: Sixty-seven adult patients (44 male, mean age 41 +/- 18 years) with the diagnosis of IVNC were evaluated in this retrospective cohort. Its prevalence was found to be .14%. Forty-seven patients (70%) had class I/II functional capacity. Fifty-seven patients (85%) had electrocardiographic abnormalities, and the most common one was left ventricular (LV) hypertrophy (25%). LV systolic function was depressed in 44 patients (66%), with a median ejection fraction (EF) of 35% (range: 20%-48%) at diagnosis. Multiple regression analysis revealed that age at initial presentation, the total number of affected segments, and the ratio of non-compaction/compaction (NC/C) were the independent predictors of LV systolic dysfunction. Familial occurrence of IVNC was 33%. During a mean follow-up of 30 months (range: 9-50 months), major complications including ventricular tachycardia, heart failure requiring hospitalization, and cerebrovascular events were observed in 36%, 34%, and 9% of the patients, respectively. Ten patients (15%) with IVNC died in this study. LVEF at initial presentation and functional capacity at last visit were found to be independent predictors of mortality. CONCLUSION: This study suggests that IVNC is a form of cardiomyopathy with higher prevalence and relatively better prognosis than previously reported. Age at initial presentation, ratio of NC/C, and number of affected segments seem to be major determinants of LV systolic dysfunction, while initial LVEF and last functional capacity predict mortality in this cohort.

Non-compaction cardiomyopathy associated with myocardial bridging: A frequently overlooked or misdiagnosed cardiomyopathy.

Isolated ventricular non-compaction (IVNC) is an unclassified cardiomyopathy which occurs due to a morphogenetic abnormality involving an arrest of compaction of the loose myocardial meshwork during fetal ontogenesis. Despite recent advances in knowledge, diagnosis remains problematic because of its similarity to other diseases of the myocardium and endocardium. In this report, we describe a case of IVNC and myocardial bridging. The patient had been misdiagnosed with apical hypertrophic cardiomyopathy 2 years earlier. The correct diagnosis was established by transthoracic echocardiography and confirmed by cardiac catheterization and angiocardiography.

Brugada-like early repolarization pattern misdiagnosed as acute anterior myocardial infarction in a patient with myocardial bridging of the left anterior descending artery.

The diagnosis of acute coronary syndrome in patients presenting to the emergency department with chest pain is still challenging. Since the symptoms and electrocardiographic abnormalities of patients with acute myocardial infarction can be indistinguishable from those of patients with other conditions that lead to ST-segment elevation, a high clinical index of suspicion is needed to avoid an incorrect diagnosis and subjecting the patient to unwarranted thrombolytic therapy. Our report concerns a 53-year-old male with myocardial bridging of the left anterior descending artery. He presented with the combined electrocardiographic abnormality of the Brugada-like or early repolarization pattern, which was misdiagnosed as acute anterior myocardial infarction.

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.

Penetrating trauma to the mitral valve and ventricular septum.

Penetrating cardiac trauma is typically life-threatening and often requires urgent surgical intervention. Penetrating injury can cause damage in more than 1 cardiac structure that may be difficult to identify at the initial urgent operation. We describe the case of a young man in whom a perimembranous ventricular septal defect and perforation of the anterior leaflet of the mitral valve were caused by a screwdriver wound.