Reversal of pulmonary vein remodeling after catheter ablation of atrial fibrillation.

BACKGROUND: Pulmonary veins (PV) and the atria undergo electrical and structural remodeling in atrial fibrillation (AF). This study aimed to determine PV and left atrial (LA) reverse remodeling after catheter ablation for AF assessed by chest computed tomography (CT). METHODS: PV electrophysiologic studies and catheter ablation were performed in 63 patients (68% male; mean ± SD age: 56 ± 10 years) with symptomatic AF (49% paroxysmal, 51% persistent). Chest CT was performed before and 3 months after catheter ablation. RESULTS: At baseline, patients with persistent AF had a greater LA volume (91 ± 29 cm(3) vs. 66 ± 27 cm(3); P = 0.003) and mean PV ostial area (241 ± 43 mm(2) vs. 212 ± 47 mm(2); P = 0.03) than patients with paroxysmal AF. There was no significant correlation between the effective refractory period and the area of the left superior PV ostium. At 3 months of follow-up after ablation, 48 patients (76%) were AF free on or off antiarrhythmic drugs. There was a significant reduction in LA volume (77 ± 31 cm(3) to 70 ± 28 cm(3); P < 0.001) and mean PV ostial area (224 ± 48 mm(2) to 182 ± 43 mm(2); P < 0.001). Patients with persistent AF had more reduction in LA volume (11.8 ± 12.8 cm(3) vs. 4.0 ± 11.2 cm(3); P = 0.04) and PV ostial area (62 mm(2) vs. 34 mm(2); P = 0.04) than those who have paroxysmal AF. The reduction of the averaged PV ostial area was significantly correlated with the reduction of LA volume (r = 0.38, P = 0.03). CONCLUSIONS: Catheter ablation of AF improves structural remodeling of PV ostia and left atrium. This finding is more apparent in patients with persistent AF treated by catheter ablation.

Giant saphenous vein graft pseudoaneurysm: treatment with a vascular occlusion device.

We report the case of a 74-year old male who was evaluated for progressively enlarging right heart border on serial chest radiographs. Computed tomography of the chest revealed a pseudoaneurysm arising from the saphenous vein graft (SVG) to the posterior descending artery with mass effect on the right atrium. Coronary angiography showed severely compromised distal flow and an angiographically small territory at risk. Using a minimally invasive, catheter-based approach, an Amplatzer Vascular Plug II occlusion device was utilized successfully for embolizing the SVG pseudoaneurysm.

Left ventricular hypertrophy: major risk factor in patients with hypertension: update and practical clinical applications.

Left ventricular hypertrophy is a maladaptive response to chronic pressure overload and an important risk factor for atrial fibrillation, diastolic heart failure, systolic heart failure, and sudden death in patients with hypertension. Since not all patients with hypertension develop left ventricular hypertrophy, there are clinical findings that should be kept in mind that may alert the physician to the presence of left ventricular hypertrophy so a more definitive evaluation can be performed using an echocardiogram or cardiovascular magnetic resonance. Controlling arterial pressure, sodium restriction, and weight loss independently facilitate the regression of left ventricular hypertrophy. Choice of antihypertensive agents may be important when treating a patient with hypertensive left ventricular hypertrophy. Angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers followed by calcium channel antagonists most rapidly facilitate the regression of left ventricular hypertrophy. With the regression of left ventricular hypertrophy, diastolic function and coronary flow reserve usually improve, and cardiovascular risk decreases.

Cardiac resynchronization therapy.

It is now well established that electrical and mechanical dyssynchrony are not clinically synonymous; however, at present no individual noninvasive method can reliably and consistently identify the criteria for mechanical dysfunction correctable through device therapy. The results of the PROSPECT (Predictors of Response to CRT) trial not only highlight the complicated nature of this dilemma, but also emphasize the importance of broadening our approach to this topic. Not only do the capabilities of real-time three-dimensional echocardiography and cardiac magnetic resonance imaging need to be maximized, but the strengths and weaknesses of each modality need to be more selectively matched to the heterogeneity of this particular patient population and subsequently studied in a robust clinical fashion.

Modulation of serum cytokine levels by a novel superoxide dismutase mimetic, M40401, in an Escherichia coli model of septic shock: correlation with preserved circulating catecholamines.

OBJECTIVES: We have shown previously that inactivation of catecholamines by superoxide anions contributes to the loss of vascular reactivity to norepinephrine and the subsequent hypotension that develops in Gram-negative endotoxic shock. In addition to their vasopressor actions, catecholamines, via beta-adrenoceptor activation, are important regulators of cytokine production. Here we examined if maintenance of serum catecholamine levels by the superoxide dismutase mimetic, M40401, modulates serum cytokine levels and arterial hypotension in an Escherichia coli-infected conscious rat model of septic shock. DESIGN: Controlled laboratory animal study. SETTING: University animal research laboratory. SUBJECTS: Pathogen-free male Sprague-Dawley rats (n = 51). INTERVENTIONS: Conscious, antibiotic-treated animals with chronic in-dwelling carotid arterial and jugular venous catheters were intravenously infected with 10(10) live E. coli bacteria (O55:B5, n = 51) over 30 mins, ending at time = 0 hrs. At 0.5 or 3 hrs, infected rats were administered an intravenous infusion of either M40401 (n = 33) or 0.9% saline (n = 18) for 6 hrs at a rate of 1 mL/h. In additional experiments, anesthetized animals with catheterized left femoral arteries and veins were administered a dose-range of norepinephrine (0.1-1 microg/kg) as bolus intravenous injections. Thereafter, E. coli lipopolysaccharide (4 mg/kg, n = 6) was administered as a 0.3-mL slow bolus intravenous injection. One hour later, the norepinephrine protocol was repeated, after which the rats were administered an intravenous infusion of either M40401 or 0.9% saline for 15 mins. At 2 hrs, the dose response to norepinephrine was repeated. MEASUREMENTS AND MAIN RESULTS: Rats infected with live E. coli exhibited a biphasic fall in mean arterial pressure, with mortality reaching 83% by 24 hrs. Rats treated with M40401 (0.25, 2.5, or 25 microg x kg-1 x hr-1 ) 3 hrs after bacteremic sepsis maintained a normal mean arterial pressure, and mortality was dose-dependently reduced to 44, 33, and 22%, respectively, at 24 hrs. Furthermore, serum catecholamine levels were diminished in E. coli-infected rats treated with saline compared with rats treated with M40401. In separate experiments, E. coli-infected rats were administered M40401 (25 microg x kg-1 x hr-1 ) 0.5 hr after bacterial challenge. Blood samples taken at 0, 1.5, 3.5, and 6 hrs were analyzed for tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, and IL-10 and for norepinephrine and epinephrine. Serum levels of tumor necrosis factor-alpha and IL-1 beta were significantly depressed in M40401-treated septic rats, whereas IL-10 was elevated. Moreover, serum catecholamine levels were greater in M40401-treated septic rats at the same time points. IL-6 levels were unaffected by M40401 treatment. Finally we examined whether treatment with M40401 could reverse the hyporeactivity to norepinephrine typifying early septic shock. Using the E. coli lipopolysaccharide (4 mg/kg) challenged anesthetized rat model of shock, we demonstrated that the vasoconstrictor ability of norepinephrine was indeed restored after M40401 treatment (25 microg/kg). CONCLUSION: Postinfection treatment with the superoxide dismutase mimetic M40401 protects against hypotension, vascular hyporeactivity to catecholamines, and mortality associated with septic shock. Such beneficial effects correlate with both reduced oxidative inactivation of serum catecholamines and a reduction in canonical cytokine mediators of inflammation.