Objective To summarize data on atrial fibrillation (AF) detection rates and predictors across different rhythm monitoring strategies in patients with cryptogenic stroke (CS) or embolic stroke of undetermined source (ESUS). Methods MEDLINE, Embase, and Web of Science were searched to identify all published studies providing relevant data through July 6, 2020. Random-effects meta-analysis method was used to pool estimates. Results We included 47 studies reporting on a pooled population of 8,215 patients with CS or ESUS. Using implantable cardiac monitor (ICM), the pooled rate of AF was 12.2% (95% CI 9.4–15.0) at 3 months, 16.0% (95% CI 13.2–18.8) at 6 months, 18.7% (95% CI 15.7–21.7) at 12 months, 22.8% (95% CI 19.1–26.5) at 24 months, and 28.5% (95% CI 17.6–39.3) at 36 months. AF rates were significantly higher in patients with ESUS vs CS (22.0% vs 14.2%; p < 0.001) at 6 months, and in studies using Reveal LINQ vs Reveal XT ICM (19.1% vs 13.0%; p = 0.001) at 12 months. Using mobile cardiac outpatient telemetry (MCOT), the pooled rate of AF was 13.7% (95% CI 10.2–17.2) at 1 month. Predictors of AF detection with ICM included older age, CHA 2 DS 2 -VASc score, left atrial enlargement, P wave maximal duration and prolonged PR interval. Conclusion The yield of ICM increases with the duration of monitoring. More than a quarter of patients with CS or ESUS will be diagnosed with AF during follow-up. About one in seven patients had AF detected within a month of MCOT, suggesting that a non-invasive rhythm monitoring strategy should be considered before invasive monitoring.

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This study investigates the effects of methylenedioxymethamphetamine (MDMA) and amphetamine on monoamine release from rat superfused brain slices in both the presence and absence of vesicular stores of transmitter. MDMA caused the release of radioactivity from slices incubated with [3H]5-hydroxytryptamine, [3H]noradrenaline or [3H]dopamine with EC50 values of 1.9 mumol/l (95% confidence limits 1.5-2.3 mumol/l), 4.5 mumol/l (2.3-8.7 mumol/l), and greater than 30 mumol/l, respectively. In contrast, amphetamine (0.1-300 mumol/l) was more effective in releasing radioactivity from slices incubated with [3H]dopamine than [3H]noradrenaline or [3H]5-hydroxytryptamine. When Ca2+ was excluded from the superfusion fluid, the MDMA-induced release of radioactivity from slices incubated with [3H]dopamine was unaltered, but that from slices incubated with [3H]noradrenaline or [3H]5-hydroxytryptamine was enhanced. MDMA (10 mumol/l) facilitated the stimulation-induced (5 Hz, 1 min) outflow of radioactivity from slices incubated with [3H]noradrenaline or [3H]5-hydroxytryptamine to 7.5-fold and 2.1-fold of control values, respectively, but had no effect on that from slices incubated with [3H]dopamine. Amphetamine (1 mumol/l) increased the stimulation-induced outflow from slices incubated with [3H]noradrenaline, but not that from slices incubated with [3H]5-hydroxytryptamine or [3H]dopamine. Inhibition of monoamine oxidase by a 30-min incubation with pargyline (100 mumol/l) enhanced the releasing action of MDMA on all three monoamines. Pargyline (100 mumol/l) also enhanced the facilitation caused by MDMA, of the stimulation-induced outflow of radioactivity from slices incubated with [3H]noradrenaline, [3H]5-hydroxytryptamine or [3H]dopamine. In some experiments, slices were obtained from reserpinised rats (2.5 mg/kg s.c. 24 h prior) and pre-exposed for 30 min to the monoamine oxidase inhibitor parglyine (100 mumol/l). Under these conditions, electrical stimulation evoked a small residual stimulation-induced outflow of radioactivity from slices incubated with [3H]noradrenaline, and failed to evoke an outflow of radioactivity from slices incubated with [3H]5-hydroxytryptamine or [3H]dopamine. However, a Ca(2+)-dependent stimulation-induced outflow of radioactivity was evoked in the presence of either MDMA (10 mumol/l) or amphetamine (1 mumol/l) from slices incubated with either [3H]dopamine or [3H]noradrenaline, but not from slices incubated with [3H]5-hydroxytryptamine. The stimulation-induced outflow of radioactivity from slices incubated with [3H]noradrenaline was enhanced in the presence of desipramine (1 mumol/l), however this enhancement was less than that caused by 10 mumol/l MDMA or 1 mumol/l amphetamine. The Ca(2+)-dependent response to electrical stimulation in the presence of MDMA from slices incubated with [3H]noradrenaline was greatly reduced when rats were pretreated with a higher dose of reserpine (10 mg/kg s.c.).(ABSTRACT TRUNCATED AT 400 WORDS)

The aim of this study was to investigate the actions of methylenedioxymethamphetamine (MDMA) in several isolated cardiovascular tissues. In spontaneously beating rat atria, concentration-dependent positive chronotropic responses to MDMA and amphetamine were blocked by the neuronal-uptake inhibitor desipramine (1 microM) and the beta-adrenoceptor antagonist propranolol (1 microM). In atria incubated with [3H]noradrenaline to label transmitter stores, 10 microM MDMA and 1 microM amphetamine increased the resting outflow of radioactivity, while 1 microM desipramine had no effect on resting outflow. The MDMA- and amphetamine-induced release of radioactivity were blocked by 1 microM desipramine. MDMA, amphetamine and desipramine each enhanced the electrical stimulation-induced (2 Hz, 30-s train) release of radioactivity; the enhancing effects of MDMA and amphetamine were blocked by 1 microM desipramine. In rat isolated perfused hearts, MDMA (1 and 10 microM) increased heart rate by a similar amount to the increase caused by noradrenaline (10 and 50 nM). MDMA also induced dysrhythmias in 7 out of 11 rat isolated perfused heart preparations. In rabbit isolated perfused and superfused ear arteries preloaded with [3H]noradrenaline, MDMA increased the resting release of radioactivity by 230 +/- 18% (n = 6) of control resting release; the increase was accompanied by a rise in perfusion pressure of 17 +/- 7 mmHg (n = 6). MDMA also facilitated the vasoconstrictor responses to noradrenaline (3-9 ng) and perivascular nerve stimulation (1-5 Hz, 10-s train). MDMA-induced vasoconstriction and the facilitation of vasoconstrictor responses to noradrenaline and electrical stimulation were blocked by 1 microM desipramine.(ABSTRACT TRUNCATED AT 250 WORDS)

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