Tularemia - a re-emerging disease with growing concern.

Tularemia caused by Gram-negative, coccobacillus bacterium, Francisella tularensis, is a highly infectious zoonotic disease. Human cases have been reported mainly from the United States, Nordic countries like Sweden and Finland, and some European and Asian countries. Naturally, the disease occurs in several vertebrates, particularly lagomorphs. Type A (subspecies tularensis) is more virulent and causes disease mainly in North America; type B (subspecies holarctica) is widespread, while subspecies mediasiatica is present in central Asia. F. tularensis is a possible bioweapon due to its lethality, low infectious dosage, and aerosol transmission. Small mammals like rabbits, hares, and muskrats are primary sources of human infections, but true reservoir of F. tularensis is unknown. Vector-borne tularemia primarily involves ticks and mosquitoes. The bacterial subspecies involved and mode of transmission determine the clinical picture. Early signs are flu-like illnesses that may evolve into different clinical forms of tularemia that may or may not include lymphadenopathy. Ulcero-glandular and glandular forms are acquired by arthropod bite or handling of infected animals, oculo-glandular form as a result of conjunctival infection, and oro-pharyngeal form by intake of contaminated food or water. Pulmonary form appears after inhalation of bacteria. Typhoidal form may occur after infection via different routes. Human-to-human transmission has not been known. Diagnosis can be achieved by serology, bacterial culture, and molecular methods. Treatment for tularemia typically entails use of quinolones, tetracyclines, or aminoglycosides. Preventive measures are necessary to avoid infection although difficult to implement. Research is underway for the development of effective live attenuated and subunit vaccines.

Stiff left atrial syndrome after catheter ablation for atrial fibrillation: clinical characterization, prevalence, and predictors.

BACKGROUND: There have been no studies of atrial diastolic function after catheter ablation of atrial fibrillation (AF). We encountered a few patients with symptomatic left atrial (LA) diastolic dysfunction and associated pulmonary hypertension (PH) that developed after catheter ablation for atrial fibrillation. Similar findings were described in patients after cardiac surgery and were referred to as the "stiff left atrial syndrome." OBJECTIVE: The purpose of this study was to prospectively quantify the incidence of patients developing PH associated with diastolic hemodynamic abnormalities of the LA after radiofrequency ablation of AF and to identify the possible predictors. METHODS: Between January 2009 and July 2010, data on 1,380 consecutive patients were prospectively collected. Before ablation and at follow-up, all patients had an echocardiogram to assess for the presence of PH. Patients with no echocardiographic evidence of PH but complaining of unexplained dyspnea with LA diastolic abnormalities were evaluated with right heart catheterization (RHC). Patients were included in the analysis if they developed new or worsening PH postablation with evidence of LA diastolic dysfunction by RHC or direct LA pressure measurement. All patients were evaluated for pulmonary vein stenosis and excluded if this condition was identified. RESULTS: The mean age was 62 ± 11 (75% male), and nonparoxysmal AF was the predominant arrhythmia (71%). New or worsening PH with associated LA diastolic abnormalities was detected in 19 (1.4%) patients after ablation. The prevalence of PH did not differ between AF types (P = .612). Compared with patients who did not develop PH, LA scarring (P <.001), diabetes (P = .026), and obstructive sleep apnea (OSA; P = .006) were more frequently observed among those who developed PH. In a multivariable logistic model, preprocedure LA size ≤45 mm (odds ratio [OR] = 6.13; P = .033), mean LA pressure (OR 1.14; P = .025), severe LA scarring (OR = 4.4; P = .046), diabetes mellitus (OR = 9.5; P = .004), and OSA (OR = 6.2; P = .009) were independently associated with the development of PH postablation. CONCLUSIONS: After radiofrequency catheter ablation of atrial fibrillation (RFCAF), PH with LA diastolic dysfunction or the so-called stiff LA syndrome is a rare but potentially significant complication of AF ablation. Severe LA scarring, LA ≤45 mm, diabetes mellitus, OSA, and high LA pressure are clinical variables that predict the development of this syndrome. The main clinical findings include dyspnea, congestive heart failure, PH, and large V waves on pulmonary capillary wedge pressure (PCWP) or LA pressure tracings in the absence of mitral regurgitation.

Pulmonary vein antrum isolation for atrial fibrillation on therapeutic coumadin: special considerations.

Pulmonary vein antrum isolation (PVAI) has emerged as an effective treatment for drug-refractory atrial fibrillation (AF). However, thromboembolic events are important complications of this approach. Management of anticoagulation is essential to prevent thromboembolic complications and avoid bleeding complications. The purpose of this review is to outline the general principles followed at our AF centers to address the important issue of pre-, peri-, and postprocedural anticoagulation strategies during PVAI of AF. We initiate warfarin therapy prior to the ablation procedure and continue it through the procedure. Prior work has demonstrated that continuation of therapeutic warfarin during the radiofrequency catheter ablation reduces the risk of periprocedural stroke/transient ischemic attack without increasing the risk of hemorrhagic events. In fact, a strategy that interrupts warfarin anticoagulation may increase the risk of stroke, even with bridging with enoxaparin. Data from our work have shown that minor bleeding was more frequent in the patients bridged with heparin or enoxaparin. There was no significant difference in incidence of major bleeding complications among the patients with a therapeutic level of international normalized ratio (INR) compared with patients for whom bridging therapy was used. Furthermore, the strategy of ablation during a therapeutic INR could be more economical compared with bridging therapy with enoxaparin. Continuation of therapeutic warfarin during ablation of AF may be the best strategy, especially in patients with nonparoxysmal AF, patients with higher thromboembolic risk scores, and patients who require extensive ablation during PVAI of AF.

Risk Stratification for Sudden Cardiac Death: The Need to Go Beyond the Left Ventricular Ejection Fraction.

Sudden cardiac death (SCD) accounts for as many as 450,000 deaths yearly in the United States. Over the last 15 years, many clinical trials have established the effectiveness of an implantable cardioverter-defibrillator (ICD) in reducing sudden and total mortality in patients with structural heart disease. However, controversy remains about exactly how to identify the patients most likely to benefit from an ICD, as well as those who may safely do without an ICD implant. The first primary prevention ICD trials used an abnormal electrophysiological study in addition to a low left ventricular ejection fraction (LVEF) as high-risk markers for SCD. More recent ICD trials selected patients based on the presence of a low LVEF alone. Ideally, noninvasive electrophysiological markers that more directly reflect arrhythmia substrates may better identify patients for prophylactic ICD implant. Several of these markers have been associated with the risk of SCD, but all have yielded contradictory outcome results or have not been tested prospectively. This review focuses on the most promising tests to date, their clinical significance, and their possible use to improve efficacy and efficiency of risk stratification for SCD.

Risk stratification using stress echocardiography: incremental prognostic value over historic, clinical, and stress electrocardiographic variables across a wide spectrum of bayesian pretest probabilities for coronary artery disease.

OBJECTIVES: We sought to evaluate the risk stratification ability and incremental prognostic value of stress echocardiography over historic, clinical, and stress electrocardiographic (ECG) variables, over a wide spectrum of bayesian pretest probabilities of coronary artery disease (CAD). BACKGROUND: Stress echocardiography is an established technique for the diagnosis of CAD. However, data on incremental prognostic value of stress echocardiography over historic, clinical, and stress ECG variables in patients with known or suggested CAD is limited. METHODS: We evaluated 3259 patients (60 +/- 13 years, 48% men) undergoing stress echocardiography. Patients were grouped into low (<15%), intermediate (15-85%), and high (>85%) pretest CAD likelihood subgroups using standard software. The historical, clinical, stress ECG, and stress echocardiographic variables were recorded for the entire cohort. Follow-up (2.7 +/- 1.1 years) for confirmed myocardial infarction (n = 66) and cardiac death (n = 105) was obtained. RESULTS: For the entire cohort, an ischemic stress echocardiography study confers a 5.0 times higher cardiac event rate than the normal stress echocardiography group (4.0% vs 0.8%/y, P < .0001). Furthermore, Cox proportional hazard regression model showed incremental prognostic value of stress echocardiography variables over historic, clinical, and stress ECG variables across all pretest probability subgroups (global chi2 increased from 5.1 to 8.5 to 20.1 in the low pretest group, P = .44 and P = .01; from 20.9 to 28.2 to 116 in the intermediate pretest group, P = .47 and P < .0001; and from 17.5 to 36.6 to 61.4 in the high pretest group, P < .0001 for both groups). CONCLUSIONS: A normal stress echocardiography portends a benign prognosis (<1% event rate/y) in all pretest probability subgroups and even in patients with high pretest probability and yields incremental prognostic value over historic, clinical, and stress ECG variables across all pretest probability subgroups. The best incremental value is, however, in the intermediate pretest probability subgroup.