Santosh K. Padala

Impact of early initiation of corticosteroid therapy on cardiac function and rhythm in patients with cardiac sarcoidosis

BACKGROUND There is limited data on the effect of corticosteroid therapy in patients with cardiac sarcoidosis (CS). We sought to examine the impact of early initiation of corticosteroid therapy, within a month of CS diagnosis, on left ventricular ejection fraction (LVEF), ventricular arrhythmias (VAs), and atrioventricular (AV) block. METHODS We retrospectively identified 30 CS patients from a large university sarcoidosis clinic. The effect of early initiation of corticosteroid therapy on LVEF was assessed by serial echocardiography, and on VAs and AV block was assessed by Holter monitoring and/or device interrogations. RESULTS The median time from diagnosis of extra-cardiac sarcoidosis to CS was 40months. 90% (27/30) of the CS patients received corticosteroid therapy and 85% percent (23/27) had early initiation of corticosteroid therapy. Fourteen patients (47%) had reduced EF<50%. 9/14 patients who had early initiation of corticosteroid therapy had improvement in mean EF (25% to 46%, P<0.001); 5/14 patients who had a delay in initiation or who did not receive corticosteroids had no improvement in mean EF (41% to 37%, P=0.47). Fourteen patients (47%) had VAs and 5 patients (17%) had advanced AV block. Early initiation of corticosteroid therapy resulted in no VA recurrences in 8/11 patients (72%), and complete recovery of AV conduction in 2/3 patients (67%). Patients with VAs (n=3) or advanced AV block (n=2) who failed to receive early corticosteroid therapy did not show improvement. CONCLUSIONS There is often a delay in manifestation of cardiac sarcoidosis for several years from the diagnosis of extra-cardiac sarcoidosis. Prompt initiation of corticosteroid therapy in CS patients may improve outcomes whereas delayed initiation of corticosteroids or failure to use corticosteroids may be associated with worse outcomes.

Stellate ganglion blockade and bilateral cardiac sympathetic denervation in patients with life‐threatening ventricular arrhythmias

Autonomic modulation is being increasingly employed as a strategy to treat ventricular arrhythmias refractory to beta‐blockers, antiarrhythmic drugs, and catheter‐based ablation procedures. We report 6 patients with refractory ventricular tachycardia (VT) or ventricular fibrillation (VF) treated with stellate ganglion blockade (SGB) and/or bilateral cardiac sympathetic denervation (CSD). Our case series emphasizes the concept that the cardiac sympathetic nerves are important targets in the management of ventricular arrhythmias. SGB and CSD can be effective in suppressing VT/VF and can be offered to patients with refractory ventricular arrhythmias as an adjunct to conventional therapy.

Intermittent loss of capture in a His bundle pacemaker: What is the cause?

Case report A 34-year-old man with a history of congenital complete heart block who underwent dual-chamber pacemaker implant at age 6 and multiple generator changes was referred for device replacement and lead extraction owing to malfunctioning atrial and ventricular leads. He underwent lead extraction of a dual-chamber pacing system with subsequent reimplantation of a Medtronic Viva CRT pacemaker (CRTP) generator and bipolar active fixation leads in the right atrium, right ventricle, and His bundle (LV port). The sensing, pacing threshold, and impedance measurements for all 3 leads were stable. On postoperative day 1, to promote His bundle–only pacing without RV pacing, the device was reprogrammed to have a subthreshold RV output of 0.50 V at 0.03 ms. Device parameters are shown in Table 1. On postoperative day 2, rhythm strips were obtained (Figure 1) on telemetry. What is the cause of intermittent loss of capture, and what programming changes would be most appropriate to resolve the issue?

His Bundle Pacing: The Holy Grail of Pacing?

C ardiac pacing has been the cornerstone of therapy for management of bradyarrhythmias since the early 1960s. For decades, right ventricular (RV) apical pacing was the primary strategy to improve survival and quality of life in patients requiring permanent ventricular pacing. The deleterious effects of long-term RV apical pacing on left ventricle (LV) function have been documented by several large prospective studies. In the DAVID (Dual Chamber and VVI Implantable Defibrillator) trial, patients with LV dysfunction randomized to a dualchamber pacing mode (DDDR) with a baseline pacing rate of 70 beats/min had a significantly higher primary composite endpoint of death or heart failure (HF) hospitalization than patients randomized to a singlechamber ventricular pacing mode (VVI) with backup pacing at 40 beats/min (1). Similar findings were reported in a substudy of the MOST (MOde Selection Trial), where >40% RV apical pacing was strongly associated with increased incidence of HF hospitalization and atrial fibrillation, even though most patients had normal cardiac function (2). Worse outcomes are associated with increased RV apical pacing, especially in patients with HF primarily attributed to intraand interventricular dyssynchrony created by nonphysiologic activation of the ventricles (3). Furthermore, chronic RV apical pacing has also been shown to result in left atrial remodeling and impair atrial function, predisposing to atrial arrhythmias (4–6). The quest for an optimal ventricular pacing site to curtail these potential adverse outcomes has been

Pulmonary Vein Stenosis After Atrial Fibrillation Ablation: An Iatrogenic Problem Larger Than the Primary Problem

See Article by Raeisi-Giglou et al Catheter-based ablation procedures for patients with symptomatic atrial fibrillation (AF) have steadily increased over the past decade in the United States. Despite significant technological advances and better understanding of the anatomic substrate, AF ablation can still result in rare, yet life-threatening complications. One such complication is pulmonary vein stenosis (PVS) and can incur substantial patient morbidity with recalcitrant symptoms. The incidence of severe PVS has fallen dramatically from 42.4% reported in an early study from 19991 to between 0.29% and 3.4% in studies after 2000.2–7 A high index of suspicion is required as presentation is often delayed (weeks to months after ablation), atypical, and can mimic a case of bronchitis, pneumonitis, or malignancy.8,9 Symptoms depend on the number of pulmonary veins involved, lesion severity, and presence and extent of collaterals. Diagnosis is often delayed or missed, as routine imaging after ablation is not mandated by the current Heart Rhythm Society consensus statements.10 If not recognized early, PVS may progress rapidly and result in total pulmonary venous occlusion, chronic pulmonary hypertension, irreversible lung parenchymal damage, and its sequelae.11,12 Treatment of PVS is also challenging and far from ideal. Pulmonary venous interventions using balloon angioplasty or stenting have been reported from single-center studies, but outcomes have remained suboptimal.13–17 Restenosis rates requiring reintervention are significant and observed in 56% to 72% of the balloon angioplasty cases compared with 27% to 33% of the stenting cases.13,14 Recently, surgical repair of severe PVS has been reported in a small series, with a restenosis rate of 38% over long-term follow-up.18 In this issue of the Circulation: Arrhythmia and Electrophysiology , Raeisi-Giglou et al19 present the Cleveland Clinic experience of outcomes and …

The Right-Sided ECG for the Right Diagnosis

A 64-year-old woman with a history of diabetes mellitus and hypertension presented to the emergency department with substernal chest pressure radiating to her back and left breast. Blood pressure was equal in both arms, and she was diagnosed with acute myocardial infarction. Despite adequate stent deployment resulting in excellent epicardial coronary artery flow, she developed confusion, hypotension, cool extremities, and an elevated serum lactate. The right-sided ECG in Figure 1 was obtained when she became hemodynamically unstable. Identify all the ECG abnormalities and the best management at this point. Figure 1. Right-sided ECG performed in a hemodynamically unstable patient. V3R through V6R are placed in their standard position along the right chest wall. Please turn the page to read the diagnosis. The right-sided ECG presented in Figure 1 shows atrial fibrillation with acute infero-posterior wall ST-segment–elevation myocardial infarction with right ventricular (RV) infarction. This ECG shows remarkable ST-segment elevations in the inferior and right-sided leads with reciprocal …

Alternating Bundle-Branch Block: What Is the Mechanism?

A 37-year-old woman with non-Hodgkin lymphoma undergoing chemotherapy and no other significant medical history was incidentally noted to have an irregular heart rhythm on physical examination, and a 12-lead ECG was obtained. ECG (Figure 1) showed sinus rhythm with alternating pattern of right bundle-branch block (RBBB) and left bundle-branch block (LBBB). What is the mechanism of the alternating bundle-branch block pattern noted on the ECG? Figure 1. Twelve-lead ECG showing sinus rhythm with alternating right and left bundle-branch block pattern of ventricular conduction. 1. Alternating RBBB and LBBB premature ventricular contractions 2. Alternating phase 3 block in the bundle branches 3. Alternating phase 4 block in the bundle branches 4. Interpolated premature ventricular contractions with alternating bundle-branch morphologies Please turn the page to read the diagnosis. Irregular heart rhythm in this patient is the result of frequent atrial ectopic beats occurring in a bigeminal fashion. P waves are seen within the preceding T waves during ectopy, and the atrial coupling interval is constant (440 ms), which confirms that these are premature atrial …

RISK SCORE MODEL FOR PREDICTING OCCURRENCE OF COMPLICATIONS IN PATIENTS UNDERGOING ATRIAL FIBRILLATION ABLATION

Background: Individual predictors of complications associated with atrial fibrillation (AF) ablation have been documented. The prognostic impact of their coexistence has not been explored. Methods: The National Inpatient Sample database was utilized to identify 106,105 patients who underwent AF

Wide Complex Tachycardia on Telemetry: What Is the Diagnosis?

A 76-year-old woman with a history of hypertension, diabetes mellitus, dilated nonischemic cardiomyopathy (ejection fraction of 35%), and normal pressure hydrocephalus for which she had received a ventriculoperitoneal shunt 5 years ago was found unresponsive at home. She was intubated for airway protection in the field and was admitted to an outside hospital where an extensive neurological workup did not reveal the cause of her unconsciousness. She was transferred to our hospital to evaluate a potential cardiac etiology for her symptoms. On admission, she was noted to have an incessant wide complex tachycardia at a rate of ≈230 beats per minute on telemetry (Figure 1A and 1B). What is the most likely diagnosis, and what is the cause for the intermittent pauses during tachycardia? Please turn the page to read the diagnosis. Figure 1. Telemetry strip showing a wide complex tachycardia. A and B show a wide complex tachycardia at a rate of ≈230 beats per minute with intermittent pauses. Differential diagnosis of this wide complex tachycardia included supraventricular tachycardia with aberrancy (functional or preexisting bundle-branch block), preexcited tachycardia (antidromic tachycardia …

Intermittent failure to capture: What is the mechanism?

Case report An 82-year-old Caucasian female patient, who had a history of hypertension, dual-chamber pacer implantation for paroxysmal atrial fibrillation, and sick sinus syndrome 3 years ago, was transferred from an outside hospital for evaluation and management of a wide complex tachycardia at 115 beats per minute (bpm). Her home medications included candesartan-hydrochlorothiazide (32/12.5 mg daily), flecainide (100 mg twice daily), metoprolol tartrate (25 mg twice daily), and amiodarone (200 mg daily). She was started on doxycycline for left foot infection 4 days prior to the admission, which resulted in nausea and multiple episodes of vomiting. She was hemodynamically stable. Initial laboratory test results were pertinent to acute kidney injury, with serum bicarbonate level of 12 mmol/L (normal range 17–29 mmol/L), blood urea nitrogen level of 63 mg/dL (normal range 8–23 mg/dL), and serum creatinine concentration of 2.5 mg/dL (normal 0.5–1.0 mg/dL). Her presenting electrocardiogram (ECG) showed a wide complex rhythm with intermittent loss of ventricular capture (Figure 1A). What is the mechanism of this intermittent failure to capture? The initial ECG (Figure 1A) showed a very wide complex tachycardia (QRS duration of 240 ms) at 115 bpm with group beating due to intermittent failure to capture. An examination of the lead V1 results demonstrated P waves preceding every QRS complex, which was consistent with P