The ECG findings during sudden collapse (syncope or sudden death) in severe aortic stenosis (AS) are not well defined. We conducted a comprehensive review of the literature for ECG data during sudden collapse in patients with AS and provided a case report of our own. There were 37 published cases of syncope or sudden death in patients with severe AS which were documented by ECG. Brady- or ventricular arrhythmias were documented in 34 cases (92%). Bradyarrhythmia (n = 24; 71%) was more common at the time of collapse than ventricular tachyarrhythmia (n = 10; 29%). There was slowing of the sinus rate before bradyarrhythmia in the vast majority of patients with bradyarrhythmia but not in those presenting with ventricular tachyarrhythmia (75% vs 0%; p <0.001). ECG evidence of ischemia (ST-segment depression or elevation) was present in most patients with bradyarrhythmia but not in those with ventricular tachyarrhythmia (75% vs 0%; p = 0.011). In conclusion, our findings suggest that left ventricular baroreceptor activation plays a dominant role in the pathophysiology of sudden collapse in patients with severe AS and suggest that ischemia may play a role as well.

Echocardiography has emerged as an essential tool to guide targeted, transcatheter biopsy of cardiac masses. Options for imaging include transthoracic or transesophageal echocardiography and intracardiac echocardiography, with appropriate use being dictated by specific patient characteristics and institutional experience. The authors present a case of three-dimensional (3-D) transesophageal echocardiography-guided transcatheter biopsy of a right ventricular mass and review the current use of echocardiography to guide these procedures.

A 17-year-old African-American female patient was referred to our institution to evaluate an incidentally diagnosed murmur. She lacked stigmata of chronic illness and had no abnormalities on examination other than a flow murmur at the left and right upper sternal borders. She had occasional sharp,

In this article we discuss two cases that highlight possible complications of cardiac device implantation. In particular, our first case involves a patient who, during implantable cardioverter defibrillator (ICD) implantation, sustained injuries to her subclavian artery and vein and subsequently developed a self-resolving neuropraxia of the brachial plexus. In our second case, the patient, also during ICD implantation, had his left cephalic vein nicked during cutdown. Post-op he then developed a hematoma-induced left brachial plexus injury that also eventually self-resolved. A literature search has not shown other incidences of iatrogenic brachial plexus injuries from ICD implantation as described.

We report a case of a 63-year-old male who presented with complaints of 9 days of fevers up to 38.3 °C, chills and rigors, and headache of 3 - 4 days duration. He also noticed that the entire right half of his visual field was obscured. MRI of the brain revealed a 4 cm acute infarction involving the calcarine cortex of the left occipital lobe. Blood cultures grew Corynebacterium propinquum . A trans-esophageal echocardiogram revealed oscillating echodensities on the aortic valve, mitral valve, and posterior leaflet of the tricuspid valve, concerning for infective endocarditis. Repeat bubble study was consistent with a small patent foramen ovale. To the best of our knowledge, there have only been four reported cases of infection by this organism, with just two of them being infective endocarditis. There are no established guidelines for therapy. We used an Etest with minimum inhibitory concentrations (MICs) reported to guide therapy. The patient was successfully treated with 6 weeks of intravenous ceftriaxone. J Med Cases. 2017;8(4):137-140 doi: https://doi.org/10.14740/jmc2795w

HomeCirculationVol. 136, No. 8An Irregular Wide Complex Tachycardia Free AccessCase ReportPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCase ReportPDF/EPUBAn Irregular Wide Complex Tachycardia Thomas E. Watts, MD, H. Thomas McElderry, MD and G. Neal Kay, MD Thomas E. WattsThomas E. Watts From Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham. , H. Thomas McElderryH. Thomas McElderry From Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham. and G. Neal KayG. Neal Kay From Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham. Originally published22 Aug 2017https://doi.org/10.1161/CIRCULATIONAHA.117.029974Circulation. 2017;136:773–775ECG ChallengeA 66-year-old woman with a history of hypertension and persistent atrial fibrillation was referred to the Arrhythmia Clinic. Before her visit, a routine 12-lead ECG was ordered (Figure 1). The patient was asymptomatic except for minor palpitations. Her medicine regimen included apixaban, flecainide 150 mg twice daily, lisinopril, loratadine, metoprolol, and simvastatin.Download figureDownload PowerPointFigure 1. Routine 12-lead ECG recorded before a clinic visit to the electrophysiology clinic.What is the cardiac rhythm and what should be the initial treatment?Please turn the page to read the diagnosis.Response to ECG ChallengeThe ECG shows a very wide QRS complex tachycardia (QRS duration 280 ms) with variation in morphology. Following a pause of 700 ms, there are repeating sequences of 6 to 7 beats with cycle lengths of 400 to 415 ms. A second ECG demonstrated that the QRS morphology changed from a right bundle-branch block type pattern to a left bundle-branch block type pattern in lead V1 (Figure 2). On interruption of the tachycardia, atrial fibrillation with an atypical left bundle-branch block was observed followed by resumption of the wide complex tachycardia. These features are consistent with flecainide-induced, pleomorphic ventricular tachycardia.Download figureDownload PowerPointFigure 2. A 12-lead ECG recorded within minutes after the ECG in Figure 1, demonstrating ventricular tachycardia with an upright QRS in lead V1 with variable morphology in lead III for 6 beats (*). The ventricular tachycardia morphology spontaneously changes to an inverted QRS in lead V1 for 7 beats (**). Following spontaneous termination of the ventricular tachycardia, the underlying rhythm is atrial fibrillation with an atypical left bundle-branch block conduction. This is followed by the occurrence of 3 beats of an upright QRS ventricular tachycardia in lead V1 for 3 beats (*) that changes to an inverted QRS in lead V1. The patient had only minor palpitations during this period. This ECG is consistent with a pleomorphic ventricular tachycardia that is a proarrhythmic complication of flecainide therapy.An intravenous bolus of sodium bicarbonate was given in the clinic with return to atrial fibrillation (Figure 3). Prior medical records showed QRS duration of 84 ms before initiating flecainide with a normal echocardiogram and nuclear stress test. On admission to the hospital, the serum flecainide level measured 1.8 μg/mL.Download figureDownload PowerPointFigure 3. The 12-lead ECG recorded immediately following an intravenous bolus of sodium bicarbonate. The underlying rhythm is atrial fibrillation conducted with left bundle-branch block. The QRS complex remains prolonged with a duration of 180 ms, probably because of the effect of flecainide on conduction in the left bundle branch because the QRS had been normal (84 ms in duration) before initiation of flecainide.Flecainide has a high affinity for open-state Na+ channels with slow unbinding kinetics. Flecainide also blocks the rapid component of the delayed rectifier current (IKr) and reduces spontaneous sarcoplasmic reticulum Ca2+ release by inhibiting ryanodine receptors. The mechanism of flecainide-induced ventricular tachycardia is uncertain. In canine studies, ventricular tachycardia (VT) was inducible with programmed stimulation after flecainide loading in 4 of 13 healthy dogs (31%) in comparison with 15 of 19 dogs after myocardial infarction.1 Spontaneous VT occurred in 8 of 19 dogs with prior myocardial infarction but in no healthy dogs.1 Rate-dependent conduction block transverse to fiber orientation was observed.1 In the present patient, the first and subsequent beats of each sequence of VT were similar in morphology, suggesting a focal mechanism, consistent with ECG and action potential recordings from isolated perfused guinea pig hearts treated with flecainide.2 Flecainide prolongs action potential duration significantly more in the left than in the right ventricle, thereby increasing action potential duration dispersion. In animal models, the ECG morphology of the first and subsequent beats of spontaneous VT had a consistent morphology suggesting a focal mechanism.2 In the present case, the spontaneous change from a right bundle-branch block to a left bundle-branch block QRS pattern during longer episodes of VT is consistent with either reentry or induction of a second focal mechanism.VT induced by class 1C agents may be resistant to direct current cardioversion. Sodium bicarbonate is effective by increasing serum sodium concentration, thereby competing with the drug for negatively charged sodium channels. In addition, alkalinization shifts more of the drug to the negatively charged state, thereby reducing its entry into sodium channels.3Our patient was treated by discontinuation of flecainide and catheter ablation of atrial fibrillation.DisclosuresNone.FootnotesCirculation is available at http://circ.ahajournals.org.Correspondence to: G. Neal Kay, MD, Division of Cardiovascular Disease, Department of Medicine, 921 Faculty Office Tower, University of Alabama at Birmingham, Birmingham, AL 35294. E-mail [email protected]References1. Ranger S, Nattel S. Determinants and mechanisms of flecainide-induced promotion of ventricular tachycardia in anesthetized dogs.Circulation. 1995; 92:1300–1311.LinkGoogle Scholar2. Osadchii OE. Flecainide-induced proarrhythmia is attributed to abnormal changes in repolarization and refractoriness in perfused guinea-pig heart.J Cardiovasc Pharmacol. 2012; 60:456–466. doi: 10.1097/FJC.0b013e31826b86cf.CrossrefMedlineGoogle Scholar3. Bou-Abboud E, Nattel S. Relative role of alkalosis and sodium ions in reversal of class I antiarrhythmic drug-induced sodium channel blockade by sodium bicarbonate.Circulation. 1996; 94:1954–1961.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Xu Z, Chang Q and Liu R (2019) Additional Questions Regarding Wide QRS Tachycardia and Atrial Fibrillation, JAMA Internal Medicine, 10.1001/jamainternmed.2019.5081, 179:12, (1731), Online publication date: 1-Dec-2019. Rambaran K and Lehnert A (2018) Positive Inotropic Drugs and Drugs Used in Dysrhythmias A Worldwide Yearly Survey of New Data in Adverse Drug Reactions, 10.1016/bs.seda.2018.06.003, (229-241), . (2017) Flecainide, Reactions Weekly, 10.1007/s40278-017-39435-0, 1681:1, (159-159), Online publication date: 1-Dec-2017. August 22, 2017Vol 136, Issue 8 Advertisement Article InformationMetrics © 2017 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.117.029974PMID: 28827222 Originally publishedAugust 22, 2017 Keywordsflecainideventricular tachycardiadrug toxicityPDF download Advertisement SubjectsArrhythmiasElectrophysiology

Eptifibatide is a commonly and widely used drug for management of acute coronary syndrome and during percutaneous coronary intervention. It is usually well tolerated with no major adverse effects. We report a rare case of life-threatening thrombocytopenia secondary to eptifibatide along with a literature review of available evidence.

OBJECTIVES AL amyloidosis affects up to 30% of patients with multiple myeloma (MM), and cardiac involvement is associated with worse outcomes. Traditional screening modalities including EKG, echocardiography and biomarkers have limited value. The aim of this study was to evaluate the clinical and prognostic value of late gadolinium enhancement (LGE) by cardiovascular magnetic resonance (CMR) imaging in patients with plasma cell dyscrasias and suspected cardiac amyloidosis (CA). METHODS A total of 251 consecutive patients with plasma cell dyscrasias who underwent CMR were enrolled in this study. Primary endpoint was all cause mortality. Clinical, ECG, echocardiographic, biomarker and CMR predictors of mortality were analyzed. RESULTS Mean age of population was 63 ± 10 years, 36% females and 19% African Americans. During a median follow-up duration of 28 months (IQR 5-56), there were 97 deaths (39%). Patients who died were more likely to have diabetes (28% vs. 14%; P = 0.03), CAD (28% vs. 16%; P = 0.04) and CKD (33% vs. 21%; P = 0.04). With endomyocardial biopsy as the gold standard (42 (17%) patients), amyloid pattern on CMR (LGE+) had sensitivity and negative predictive values of 100%; specificity and positive predictive values of 80 and 81% with an AUC 0.9 for CA. History of CAD (HR 1.64, 95% CI 1.01-2.6; P = 0.04), brain natriuretic peptide (HR 1.0003 95% CI 1.0001-1.0006; P = 0.004) and LGE + (HR 1.72, 95% CI 1.05-2.8; P = 0.02) were independent predictors of mortality. LGE+ possessed incremental prognostic value over clinical, laboratory and echocardiographic variables for mortality prediction. CONCLUSIONS CMR is a clinically useful tool for diagnosis and prognostication in myeloma patients with suspected CA.

KEY TEACHING POINTS•Graft-versus-host disease (GVHD) may manifest over an implantable cardioverter-defibrillator implantation site.•We believe that it is important to include GVHD when cultures are negative and antibiotics have not subsided symptoms, especially in a patient who has undergone allogeneic hematopoietic cell transplantation.•Early diagnosis and treatment are critical to improve outcome of GVHD. Open table in a new tab

A 61-year-old African-American female with ischemic cardiomyopathy with left ventricular ejection fraction of less than 35% despite optimal, guidelinedirected medical therapy; New York Heart Association Class III symptoms; and left bundle branch block with QRS duration of 138 milliseconds underwent atrio-biventricular implantation of implantable cardioverter defibrillator. Patient was taking 81mg aspirin daily, but was not on any oral anti-coagulants. After placing 2 guidewires in left cephalic vein for right ventricular and right atrial lead placement, we attempted to obtain left subclavian vein access for left ventricular lead placement. However, there was difficulty cannulating subclavian vein due to clavicular bone anatomy obstructing access. Venous access was initially attempted with micropuncture needle but was unsuccessful. At one point, micro-puncture needle entered subclavian artery, as evidenced by bright, red, pulsatile flow. Needle was carefully withdrawn and direct pressure was applied for 5 minutes to achieve hemostasis. Patient’s vital signs remained stable. Subsequently, left axillary vein was accessed using micropuncture needle. Remainder of the case was uneventful and device was successfully implanted via left axillary vein. Patient tolerated the procedure well, and post-procedure vital signs were stable. She remained asymptomatic, specifically denying pleuritic chest pain and shortness of breath. Chest radiograph immediately after proce620

Patients with multiple myeloma have a high incidence of AL amyloidosis. Traditional screening modalities including EKG and echocardiography have limited value. The aim of this study was to evaluate the role of Brain Natriuretic Peptide (BNP) level in screening for cardiac amyloidosis and to evaluate

Background: Placement of a left ventricular (LV) lead can be difficult due to anatomical variations and structural heart disease, as well as valves at the coronary sinus (CS) ostium. An alternative technique is cannulating the CS temporarily via the femoral vein (FV) prior to placing the LV lead. Aim: To document whether there were differences in fluoroscopy times (FT) and procedure times (PT) utilizing an FV approach for CS cannulation in LV lead placement. Methods: We performed a retrospective chart review of 166 patients at the Zablocki VA Hospital who had initial LV lead placement per standard indications defined by current guidelines. We compared patients undergoing an FV approach versus those undergoing a standard approach. Exclusion criteria: upgrades, no data recorded, generator replacement. We included 135 patients, 60 in the FV group (including 1 patient who crossed over from the non-FV group) and 75 in the non-FV group. Two equally experienced operators were identified; one exclusively used the FV approach and the other used the standard approach plus the FV approach for right-sided implants only (n54). Results: FTs for the FV group averaged 44.4 ¡ 28.8 minutes (min) and FTs for the non-FV group averaged 39.7 ¡ 32.76 min (p50.1945). There was no statistically significant difference between groups. PTs for the FV group averaged 3.66 ¡ 1.1 hours (h) (including the average 28 min required to cannulate the CS via the FV, chest preparation and operator scrub-out and scrub-in times). PT for the non-FV group was 2.88 ¡ 1.7 h (p5,0.001). The median difference is 1.1 h longer in the FV group with a 95% median CI of (0.6, 1.5) h. There were no procedural complications including where the FV approach was utilized. Conclusions: There is no significant difference in FT between the two groups. However, there is a significant difference in the PT between the two groups, favoring a shorter PT in the non-FV group. Operator differences may have played a role in this. Furthermore, CS cannulation by the FV approach delayed the remainder of the procedure by 28 min on average, thus contributing to the longer PT in the FV group. Nevertheless, this remains a unique alternative technique that should be considered in any patient with difficult or unusual anatomy.

"Right-sided implantation of a biventricular ICD in a patient with persistent left superior vena cava: a challenging engagement." Acta Cardiologica, 70(1), pp. 84–85Persistent left superior vena cavaright-sided ICD implantationcardiac resynchronization therapy

BACKGROUND:Animal studies showed that the use of metformin after myocardial infarction (MI) resulted in a protective effect on cardiac myocytes. In this study, we examined the effect of metformin in patients with diabetes mellitus (DM) on left ventricular ejection fraction (LVEF) and post-MI mortality.METHODS:We reviewed charts of patients with MI admitted to the UAMS medical center. Baseline characteristics and 12-month follow up data were collected. Patients were classified into three groups: Control group- no DM (n = 464), Metformin group- DM + MI (n = 88) and No-Metformin group- DM + MI (n = 168). First, we compared Metformin and No-Metformin groups to the Control group. Second, we performed propensity-score matching in patients with DM, and compared Metformin to No-Metformin groups.RESULTS:All-cause 30-day and 12-month mortality was significantly higher in the No-Metformin group compared to controls (13.5 vs 9.3% p = 0.03 at 30 days, 23.7 vs 15.9 % p = 0.03 at 12 months). However, all-cause 30-day and 12-month mortality were similar in the Controls and Metformin group (9.3 vs 6.8 % p = 0.93 at 30 days, 15.9 vs 11.4 % p = 0.97 at 12 months). Mean LVEF on presentation (45 % in the three groups) and at follow up (47.84, 46.38 and 43.62 % in Control, Metformin, and No-Metformin groups, respectively) were not statistically different. There were no significant differences in regard to re-hospitalization, re-intervention, new stroke, CHF development, new MI, or identifiable arrhythmias. Metformin was an independent predictor of lower 30-day and 12-month all-cause mortality in patients with DM (HR 0.25, p = 0.02 and HR 0.32, p = 0.01, respectively). In the matched analysis, 30-day all-cause mortality was significantly higher in the No-Metformin compared to the Metformin group (21.1 vs 8.8 %, p = 0.05). However the difference in 12-month all-cause mortality did not reach statistical significance (24.6 vs 15.8 %, p = 0.15).CONCLUSION:This proof-of-concept study shows that use of metformin in patients with DM is associated with lower 30-day all-cause mortality and tendency for a lower 12-month all-cause mortality following MI without discernible improvement in LVEF.

We report a case of fatal fulminant hepatic failure related to the use of disulfiram. This is a commonly used medication; however there are few reported cases in the medical literature of fatal liver failure related to its use. Patients using disulfiram for alcohol cessation typically have multiple risk factors for liver disease and are not acutely candidates for orthotopic liver transplant due to recent alcohol dependence. This case demonstrates a rare adverse reaction to a commonly used medication with a fatal outcome. Our patient was a sixty-six year old man who had recently started using disulfiram for the purpose of alcohol cessation. He developed hepatotoxicity that progressed to fulminant hepatic failure. Despite cessation of the medication and supportive care, the outcome was fatal.

Atherogenesis has been traditionally viewed as a metabolic disease representing arterial obstruction by fatty deposits in its wall. Today, it is believed that atherogenesis involves highly specific biochemical and molecular responses with constant interactions between various cellular players. Despite the presence of inflammatory reaction in each and every step of atherosclerosis from its inception to terminal manifestation, the cause–effect relationship of these 2 processes remains unclear. In this article, we have attempted to review the role of inflammation in the development of atherosclerosis and in its major complication—coronary heart disease.