Pulmonary Congestion Complicating Atrial Fibrillation Cardioversion.

Acute pulmonary congestion (APC) may occur within hours after electrical cardioversion of atrial fibrillation (AF). There is scarce data about its incidence, risk factors, and the outcome. In the present study, data of consecutive patients admitted for first electrical cardioversion for AF between 2007 and 2016 were retrospectively reviewed. APC within the 48 hours following cardioversion was defined as dyspnea and at least one of the following: drop in saturation to <90%, administration of intravenous diuretic or an emergent chest X-ray with new pulmonary congestion. All-cause mortality was determined from the national registry. Total of 1,696 patients had first cardioversion for AF, of whom 66 (3.9%) had APC. In a multivariate logistic regression model independent predictors of APC included (OR [CI], p): older age (odds ratio [OR] 1.05, 95% confidence interval [CI] 1.02 to 1.08, p = 0.001), rapid ventricular response (OR 1.98, 95% CI 1.17 to 3.34, 0.010), previous heart failure (OR 3.53, 95% CI 2.09 to 5.97, p <0.001), Amiodarone loading (OR 2.38, 95% CI 1.18 to 4.79, p = 0.016) and diabetes mellitus (OR 1.77 95% CI 1.05 to 3.00, p = 0.033). There was no difference in cardioversion success rate (overall 94%). In-hospital mortality was 1.5% within the APC group and 0.5% without (p = 0.301). Patients with APC had higher rate of 6-month readmissions (28.8% vs 18.1% p <0.028). Within a median follow-up of 2.9 years, APC following cardioversion was an independent predictor of overall mortality (hazard ratio 1.73, 95% CI (1.17 to 2.56) p = 0.006). In conclusion, APC occurs in 3.9% of hospitalized patients following electrical AF cardioversion. Risk factors include increased age, diabetes mellitus, heart failure, Amiodarone loading and rapid ventricular response. APC following cardioversion is associated with increased rates of readmissions and mortality.

Late in-hospital pressure gradient measurements improve prediction of long-term outcome of alcohol septal ablation in hypertrophic cardiomyopathy.

BACKGROUND: Left ventricular outflow gradient is associated with increased morbidity and mortality in hypertrophic cardiomyopathy. Alcohol septal ablation is the alternative to surgery in cases refractory to drug therapy. The implication of LVOG measured 1 week post-ASA for prediction of outcome is unknown. OBJECTIVE: To observe the pattern of LVOG course and prediction of long-term clinical and hemodynamic outcome of ASA. METHODS: Baseline clinical and echocardiographic parameters were prospectively recorded in 14 consecutive patients with a first ASA, at the time of ASA, 3 and 7 days after ASA (in-hospital), and 3 and > or = 12 months after ASA (last follow-up). RESULTS: There was improvement in NYHA class, exercise parameters and LVOG in 11 of 14 patients (P < 0.005 in all). Maximal creatine kinase level was lower than 500 U/L in those without such improvement and 850 U/L or higher in successful cases. LVOG dropped from 79 +/- 30 to 19 +/- 6 mmHg after the ASA. LVOG was 50 +/- 21 mmHg on day 3, 39 +/- 26 on day 7, 32 +/- 26 at 3 months and 24 +/- 20 mmHg at last follow-up. LVOG identified 27% sustained procedural successes on day 3 and 73% on day 7. The overall predictive accuracy of the test for sustained success and failure was 36% on day 3 and 71% on day 7. Combination of maximal CK and LVOG on day 7 showed four distinct outcome patterns: "early success" with low LVOG and high CK (73% of successful cases), "late success" with high LVOG and high CK, and "early failure" and "late failure" with both low CK and high or low LVOG, respectively. CONCLUSION: LVOG measurement 7 days post-ASA combined with maximal CK levels predicts late procedural outcome in the majority of patients.

False-positive microhematuria in dipsticks urinalysis caused by the presence of semen in urine.

OBJECTIVES: Positive readings of blood in dipstick urinalysis may indicate trauma or imbalance in hemostasis associated with drug treatment. We evaluated the possibility that the presence of semen in urine may cause false-positive hematuria. DESIGN AND METHODS: Semen specimens obtained from 25 healthy men were directly applied on urine dipsticks for evaluation of the presence of blood. Isolated sperm cells and seminal fluid were also tested. Dipstick analyses were further performed with semen samples diluted in normal urine. Four healthy male volunteers provided urine samples before and immediately after having had sexual relationships. These samples were dipstick tested for the presence of blood. RESULTS: Semen, spermatozoa and seminal fluid gave false positive results for microhematuria following direct application of samples on dipsticks as well as after their suspension in urine (p < 0.00001).Three out of four postcoital urine specimens yielded positive results for blood. CONCLUSIONS: In men, postcoital urine may be falsely "positive" for microhematuria. This may have implication on the management of male patients in emergency situations such as acute coronary syndromes.