Natural history of untreated HDV patients: Always a progressive disease?

A severe course has been described in early studies on chronic hepatitis D (CHD), with faster pace towards liver cirrhosis with subsequent high liver-related morbidity and mortality in the majority of patients. Earlier studies have included risk groups as people using intravenous drugs (PWID) or those with multiple co-morbidities. During the last decade, the epidemiological landscape of CHD has changed with domestic cases decreasing while increasing cases of CHD consisting of younger persons immigrating from endemic regions to low-endemic regions. Recently, further insights into the spectrum of the disease with an indolent disease course in a substantial proportion of persons with CHD have been gained. At diagnosis, ≥30%–50% had already established liver cirrhosis. Older age, liver cirrhosis, co-infection with HIV and lack of interferon (IFN) therapy are the main predictors of worse clinical outcome. The newly introduced and upcoming antivirals against CHD are highly anticipated, considering the historically low virological response rates to antiviral therapy. Further knowledge is needed to fully comprehend the natural course and the spectrum of this severe form of viral hepatitis. This is also to be able to evaluate the long-term effects of the new antivirals on disease progression.     

Atrial fibrillation: A progressive atrial myopathy or a distinct disease?

Atrial fibrillation is a complex arrhythmia with multiple possible mechanisms. A lot of experimental and clinical studies have shed light on the pathophysiological mechanisms of arrhythmia, especially on molecular basis. Electrical, contractile and structural remodeling, calcium handling abnormalities, autonomic imbalance and genetic factors seem to play a crucial role in atrial fibrillation initiation and maintenance. However, the exact pathophysiological mechanisms of atrial fibrillation are not completely understood and whether atrial fibrillation is an unclassified cardiomyopathy or a distinct disease still remains to be answered. This review highlights proarrhythmic and pathophysiological mechanisms of atrial fibrillation and approaches the molecular basis underlying atrial fibrillation susceptibility.     

Mechanisms of atrial fibrillation: is a cure at hand?

The mechanisms of atrial fibrillation relate to the presence of random reentry involving multiple interatrial circuits. Triggers for development of atrial fibrillation include rapidly discharging atrial foci (mainly from pulmonary veins) or degeneration of atrial flutter or atrial tachycardia into fibrillation. Therapy for control of atrial fibrillation includes drugs, atrial pacing for those with sinus node dysfunction, or ablation of the atrioventricular junction. Therapeutic maneuvers for cure of atrial fibrillation include surgical or radiofrequency catheter induced linear lesions to reduce the atrial tissue and prevent the requisite number of reentrant wavelets. We need a much better understanding of basic mechanisms before a true cure is at hand.     

The optimal management of patient with permanent atrial fibrillation and heart failure with reduced ejection fraction – The permanent His-bundle pacing is a solution. A case report

Atrial fibrillation (AF) coexists frequently with heart failure (HF). Permanent His-bundle pacing (pHBP) seems to be an optimal approach to the management of patients with HF and concomitant AF, which are the indication for single chamber ICD implantation. This management allows to up-titrate the beta-blocker dose in order to prevent tachyarrhythmia with no risk of bradyarrhythmia or triggering deleterious right ventricular pacing. We present a case of 69-years-old male with AF, worsening HF and high burden of RV pacing. The upgrade from single chamber ICD to dual chamber ICD with pHBP alleviated the symptoms and contributed to substantial echocardiographic improvement.     

Antiarrhythmic drugs in patients with recurrent atrial fibrillation: where are we?

In patients with recurrent atrial fibrillation (AF), the hallmark of treatment has long been the use of antiarrhythmic drugs. The following strategies are available: a) any antiarrhythmic treatment; b) out-of-hospital episodic treatment ("pill-in-the-pocket" approach); c) prophylactic antiarrhythmic therapy; and d) hybrid therapy. The following patients with recurrent AF should not undergo any antiarrhythmic therapy: after the first AF episode; patients with rare, hemodynamically well-tolerated and short-lasting (a few hours) AF episodes; patients with perioperative AF, without history of recurrent AF; patients with AF during acute myocardial infarction or other acute diseases, without history of recurrent AF; and "holiday heart" syndrome. In patients with infrequent AF episodes (< 1 per month) and hemodynamically well-tolerated, but long enough to require emergency room intervention or hospitalization, a good treatment might be the "pill-in-the-pocket" approach, consisting of a single-dose oral ingestion of flecainide or propafenone at the time and place of palpitation onset. A recent Italian study has shown that this treatment is effective and safe. When AF episodes are frequent and/or hemodynamically badly tolerated, the treatment of choice is the prophylactic therapy with antiarrhythmic drugs. When these drugs fail (ineffective or not tolerated) a non-pharmacological treatment or a hybrid therapy may be indicated.     

Is there a role for maintaining sinus rhythm in patients with atrial fibrillation?

Recent studies have indicated that outcomes in patients with atrial fibrillation who are managed with rate control and anticoagulation are similar to those in patients who have maintenance of sinus rhythm. These studies did not include important groups of patients with atrial fibrillation in whom antiarrhythmic therapy may be appropriate. This perspective argues for the maintenance of sinus rhythm and for the use of antiarrhythmic therapy that includes medications, invasive procedures, and a combination of both in appropriate patients.     

Effect of combined spironolactone-β-blocker ± enalapril treatment on occurrence of symptomatic atrial fibrillation episodes in patients with a history of paroxysmal atrial fibrillation (SPIR-AF study)

Angiotensin II and aldosterone are key factors responsible for the structural and neurohormonal remodeling of the atria and ventricles in patients with atrial fibrillation (AF). The aim of the present study was to evaluate the antiarrhythmic effects of spironolactone compared to angiotensin-converting enzyme inhibitors in patients with recurrent AF. A cohort of 164 consecutive patients (mean age 66 years, 87 men), with an average 4-year history of recurrent AF episodes, was enrolled in a prospective, randomized, 12-month trial with 4 treatment arms: group A, spironolactone, enalapril, and a β blocker; group B, spironolactone and a β blocker; group C, enalapril plus a β blocker; and group D, a β blocker alone. The primary end point of the trial was the presence of symptomatic AF episodes documented on the electrocardiogram. At 3-, 6-, 9-, and 12 months, a significant (p < 0.001) reduction had occurred in the incidence of AF episodes in both spironolactone-treated groups (group A, spironolactone, enalapril, and a β blocker; and group B, spironolactone plus a β blocker) compared to the incidence in patients treated with enalapril and a β blocker (group C) or a β blocker alone (group D). No significant difference was seen in AF recurrences between patients taking spironolactone and a β blocker with (group A) and without (group B) enalapril. No significant differences were found in the systolic or diastolic blood pressure or heart rate among the groups before and after 1 year of follow-up. In conclusion, combined spironolactone plus β-blocker treatment might be a simple and valuable option in preventing AF episodes in patients with normal left ventricular function and a history of refractory paroxysmal AF.     

Cardioversion of atrial fibrillation with ibutilide: When is it most effective?

BACKGROUND: Atrial fibrillation (AF) is found in 1% of persons above the age of 60 years. More than 5% of the population older than 69 years and about 14% of octogenarians are at risk for this arrhythmia. It is estimated that 1.5 to 3 million persons in the United States alone suffer from AF. The public health implications and attendant morbidity are a significant drain on our health care system. HYPOTHESIS: The purpose of this study was to determine the clinical and echocardiographic predictors of success in converting AF of > or = 24 h duration. METHODS: Demographic and clinical and echocardiographic parameters of 101 patients with recent onset AF (> 24 h) who received ibutilide were studied. RESULTS: Of 101 patients, 56 (55%) converted to sinus rhythm. Age, gender, hypertension, diabetes mellitus, left ventricular ejection fraction (< or = 35%), congestive heart failure, and previous medication for rate control had no significant effect on the conversion rate. Conversion rate was only 30% (9/30 patients) in the presence of an enlarged left atrium (LA > or = 5 cm) and 37.7% (23/61 patients) in the presence of mitral valve disease (MVD), whereas the conversion rate was 82.5% (33/40 patients) in the absence of MVD and 85% (29/34 patients) in the absence of both enlarged LA and MVD (p = <0.001). Patients with coronary artery disease (CAD) also exhibited a significantly greater response to ibutilide than patients without CAD (77 vs. 46%, p-value 0.005). CONCLUSION: As a therapy for cardioversion of AF, ibutilide is most effective in a selected subgroup patients, such as in patients with CAD and in patients without MVD and/or markedly enlarged left atrium.