Eric M. Crespo

Electrical resynchronization induced by direct His-bundle pacing

BACKGROUND Biventricular pacing (BiV) to effect cardiac resynchronization therapy can be technically difficult and fails to elicit a clinical response in 30% to 40% of patients. Direct His-bundle pacing (DHBP) theoretically could obviate some of these problems. Although DHBP is capable of narrowing the QRS in some patients, the consistency with which this can be achieved has not been characterized. OBJECTIVE The purpose of this study was to restore His-Purkinje functionality in consecutive patients undergoing de novo clinically mandated cardiac resynchronization therapy. METHODS DHBP was temporarily implemented at the time of implantation of a permanent BiV system in patients referred for cardiac resynchronization therapy. Native conduction, DHBP, and BiV QRS duration were compared. All patients presenting for BiV cardiac resynchronization therapy were eligible for the study. Ten patients were studied. RESULTS DHBP was successfully implemented in all 10 patients. In 7 of 10 patients, DHBP narrowed the QRS significantly compared with native conduction and BiV (mean QRS duration: native 171 +/- 13 ms, DHBP 148 +/- 11 ms, BiV 158 +/- 21, P <.0001). QRS narrowing with DHBP was specifically attributable to capture of latent His-Purkinje tissue. DHBP lead implantation time (16 minutes) was shorter than standard left ventricular lead implantation time (42 minutes). CONCLUSION DHBP was readily implemented in patients with standard indications for BiV cardiac resynchronization therapy. In most patients studied, DHBP resulted in a significantly narrower QRS compared with native conduction. DHBP may offer a physiologic alternative to BiV for cardiac resynchronization therapy.

Evaluation and management of thrombocytopenia and suspected heparin-induced thrombocytopenia in hospitalized patients: The Complications After Thrombocytopenia Caused by Heparin (CATCH) registry

BACKGROUND Thrombocytopenia and heparin-induced thrombocytopenia (HIT) are potentially devastating paradoxical side effects of heparin therapy. We explored the evaluation, management, and clinical consequences of thrombocytopenia occurring during heparin therapy in diverse clinical settings. METHODS CATCH was a prospective observational study that enrolled 3,536 patients in 48 US hospitals. Data were collected on 3 strata: patients receiving any form of heparin for > or =96 hours (n = 2,420); cardiac care unit (CCU) patients treated with heparin who developed thrombocytopenia (n = 1,090); patients who had an HIT assay performed (n = 449). RESULTS Thrombocytopenia occurred in 36.4% of patients in the prolonged heparin stratum and was associated with an increased risk of death or thromboembolic complication (OR 1.5, 95% CI 1.2-1.9). Among a subset of patients whose clinical presentation suggested they were at high risk for HIT, suspicion for HIT was uncommon (prolonged heparin stratum 19.8%, CCU stratum 37.6%) and often did not arise until > or =1 day after patients developed thrombocytopenia. Often patients were not evaluated for HIT until after they had had a thromboembolic complication (prolonged heparin stratum 43.8%, CCU stratum 61%). Even after HIT was suspected, patients often continued to receive heparin. Direct thrombin inhibitor use was infrequent (prolonged heparin stratum 29.4%, CCU stratum 35.6%). Among the few patients who underwent evaluation, HIT was confirmed in 46.7% of the prolonged heparin stratum and 31.4% of the CCU stratum. CONCLUSIONS Thrombocytopenia is common among patients receiving heparin, and it is associated with substantial risk for catastrophic complications. Despite the high risk for HIT in this population, recognition, evaluation, and appropriate treatment are infrequent and delayed.

The Use of Implantable Cardioverter Defibrillators for the Prevention of Sudden Cardiac Death: A Review of the Evidence and Implications

Sudden cardiac death (SCD) claims approximately 460,000 lives per year in the United States, and half of these deaths occur in people with a history of coronary artery disease. Patients with left ventricular dysfunction and a history of myocardial infarction are at especially high risk. There is now strong evidence from multiple well-designed randomized controlled trials that implantable cardioverter defibrillators (ICDs) save lives when used for both primary and secondary prevention. As indications for ICD implantation have broadened, considerable debate has taken place because of the substantial cost involved in widespread ICD utilization. This article summarizes the epidemiology of SCD, reviews the evidence supporting the use of ICDs in patients with ischemic cardiomyopathy, and explores some of the controversy surrounding ICD utilization that has arisen in the wake of recent trials that have utilized ICDs for the primary prevention of SCD.

Autopsy Analysis of the Implantation Site of a Permanent Selective Direct His Bundle Pacing Lead

To date, there has not been direct visualization of the anatomic location of direct His bundle pacing (DHBP) leads in the human heart. The absence of such data has contributed to disagreement about the location of DHBP leads with respect to the plane of the tricuspid valve.1,2 We present an autopsy study of a patient who had previously had a DHBP lead implanted, showing unequivocally that the lead is implanted on the atrial side of the tricuspid annulus. An 81-year-old man with diabetes died of sepsis secondary to a lower-extremity infection. Two years prior, the patient presented with symptoms of congestive heart failure and presyncope. He had a history of coronary artery bypass graft and myocardial infarction with mild to moderate left ventricular dysfunction (ejection fraction, 40%–45%). β-blockade therapy was limited by sinus bradycardia and frequent Wenckebach block. The patient was noninducible for ventricular arrhythmias, and a pacemaker was recommended for chronotropic incompetence and AV block. To prevent pacemaker-induced electric dyssynchrony, we implanted a DHBP lead. DHBP lead implantation was performed as previously described.3 Briefly, an octapolar mapping catheter was used to map the His bundle. A pacing lead was actively fixed adjacent to bipolar electrodes recording a His potential (SelectSecure lead, model 3830, delivered …

Six-Month Follow-Up of Patients With In-Hospital Thrombocytopenia During Heparin-Based Anticoagulation (from the Complications After Thrombocytopenia Caused by Heparin [CATCH] Registry)

Thrombocytopenia is a predictor of adverse outcomes in patients with acute coronary syndromes and in critically ill patients. The Complications After Thrombocytopenia Caused by Heparin (CATCH) registry was designed to explore the incidence, management, and clinical consequences of in-hospital thrombocytopenia occurring during heparin-based anticoagulation in diverse clinical settings. We conducted a prospective observational study of 37 United States hospitals participating in the CATCH registry to assess the relation of in-hospital thrombocytopenia to long-term outcomes. A total of 2,104 patients at increased risk of developing in-hospital thrombocytopenia or thrombosis were identified, and the 6-month mortality and rehospitalization rates were determined. Thrombocytopenia was not a significant predictor of 6-month mortality. In an adjusted model for in-hospital death in this cohort, thrombocytopenia had an odds ratio of 3.59 (95% confidence interval 2.24 to 5.77). The postdischarge mortality rate at 6 months was 9.7%. No significant difference was observed in the long-term mortality between patients who developed thrombocytopenia and those who did not. Thrombocytopenia was a weak, but statistically significant, predictor of a composite of mortality and rehospitalization at 6 months (hazards ratio 0.80, 95% confidence interval 0.65 to 0.98, p = 0.03). In conclusion, the 6-month mortality rate among heparin-treated patients with thrombocytopenia is high, although the risk independently related to thrombocytopenia appears to be restricted to the acute hospital phase.

Contribution of Bleeding and Thromboembolic Events to In-Hospital Mortality Among Patients With Thrombocytopenia Treated With Heparin

In a population of patients experiencing thrombocytopenia while treated with heparin, bleeding and thromboses are well-appreciated complications, but their relative contributions to mortality have been less well described. In this population, the aims of this study were (1) to identify the independent predictors of bleeding and (2) to compare the incidence and the strength of association of bleeding and of new thromboses to in-hospital mortality. The independent predictors of bleeding and in-hospital mortality were identified using multivariate logistic regression models on the 1,478 patients who developed thrombocytopenia after their enrollment in the Complications After Thrombocytopenia Caused by Heparin (CATCH) study. The independent predictors of bleeding were chronic hematologic disorders, intra-aortic balloon pump, congestive heart failure, and platelet count nadir <120 x 10(9)/L. Although bleeding (n = 141 [10%]) and thromboembolic complications (n = 135 [9%]) were equally prevalent, the former was less strongly associated than the latter with in-hospital mortality (odds ratio 1.75, 95% confidence interval 1.01 to 3.03, and odds ratio 2.77, 95% confidence interval 1.67 to 4.61, respectively). In conclusion, medical management should be directed mainly at the prevention of thromboembolic complications, while additionally considering the risk for bleeding.

Brugada syndrome unmasked by a mosquito.

Two weeks after returning from missionary work in Haiti, a 53-year-old woman with no significant past medical history presented with 5 days of worsening fevers, chills, diaphoresis, myalgias, and severe nausea. Notably, she did not take malaria prophylaxis while in Haiti. Her temperature was 40.1 C, her blood pressure was 100/ 58 mmHg, and her heart rate was 102 beats per minute. Physical examination was remarkable only for her ill appearance. Initial lab work revealed anemia (hemoglobin, 10.4 g/dL; hematocrit, 29.4%), thrombocytopenia (23,000/mm), and evidence of acute renal failure (blood urea nitrogen, 58 mg/dL; creatinine, 4.2 mg/dL). Other labs were within normal limits. Malaria was considered high on the differential diagnosis. A parasite smear was therefore obtained, and the findings were consistent with Plasmodium falciparum infection (5.5% parasitemia). She was admitted to the intensive care unit for hydration and initiation of antimalarial therapy. Her severe nausea prevented administration of oral medications; therefore, the infectious disease consultant recommended treatment with intravenous quinidine. Prior to initiation of quinidine, an electrocardiogram (ECG) was obtained (Figure 1). No prior ECGs were available for comparison. Prominent ST segment elevation was noted, prompting reassessment of the patient. She denied chest pain. Cardiac enzymes were normal, and an urgent echocardiogram demonstrated normal ventricular function with mild mitral regurgitation. Given that suspicion for acute coronary syndrome was low, the ECG findings were managed conservatively. Overnight, she defervesced and appeared to improve clinically. Cardiac enzymes remained negative. A repeat ECG obtained several hours after admission revealed complete resolution of the ST elevation (Figure 2). Repeat ECGs remained normal through the time of discharge, and no ventricular arrhythmias were noted on telemetry. On the basis of the characteristic ECG appearance, a presumptive diagnosis of Brugada syndrome was made. The patient did not have a history of presyncope, syncope, or agonal night-time breathing or a family history of sudden death. Two weeks following discharge, she was seen in the outpatient electrophysiology clinic to discuss further risk stratification. A procainamide challenge, followed by programmed ventricular stimulation (electrophysiology study), was recommended. The procainamide challenge revealed ST segment changes consistent with Brugada syndrome. She was not inducible for ventricular arrhythmias during the electrophysiology study. On the basis of these findings as well as her lack of symptoms, there was no indication for an implantable cardioverter defibrillator.