The relationship between paroxysmal atrial fibrillation and coronary artery spasm.

BACKGROUND: Coronary artery spasm has recently been reported as a complication of the ablation of atrial fibrillation (AF). It may be induced by cardiac autonomic nervous dysfunction during radiofrequency catheter ablation of AF. However, the underlying mechanism is not clear. We hypothesized that patients with paroxysmal AF coincidentally exhibit coronary artery spasm. METHODS: A total of 51 patients were enrolled in a case control study to clarify the relationship between paroxysmal AF and coronary artery spasm. We evaluated 17 patients with paroxysmal AF (AF group) and 34 patients without paroxysmal AF (control group). Drug-induced coronary artery spasm provocation tests were performed by intracoronary administration of acetylcholine or ergonovine. RESULTS: The AF group consisted of nine males and eight females, mean age 67 ± 10 years. The control group consisted of 16 males and 18 females, mean age 60 ± 14 years. In the AF group, coronary artery spasm was induced in 13 patients (76.5%) before AF ablation. In the control group, coronary artery spasm was induced in three patients (8.8%). Coronary artery spasm was more frequently induced in patients with AF (76.5% vs 8.8%; odds ratio, 33.583; 95% confidence interval, 6.5732-171.58; P < 0.0001). In the AF group, ventricular fibrillation and AF were recorded immediately after right coronary artery spasm induction in one patient. CONCLUSIONS: Paroxysmal AF patients have high positive rates of drug-provoked coronary artery spasm. Patients with paroxysmal AF may coincidentally exhibit coronary artery spasm.

Resolution of left atrial appendage thrombus with apixaban.

Left atrial appendage (LAA) thrombosis is an important cause of cardiogenic cerebral thromboembolism. Apixaban is a member of the class of novel oral anticoagulants (NOAC) and is superior to warfarin in preventing stroke or systemic embolism, causes less bleeding, and results in lower mortality in patients with atrial fibrillation. There are few reports of resolution of LAA thrombus with other NOAC. We present a 72-year-old male patient with persistent atrial fibrillation associated with left atrial thrombus. Sixteen days of apixaban treatment showed complete thrombus resolution. In this study, soluble fibrin and D-dimer levels decreased without prolongation of international normalized ratio (INR) and activated partial thromboplastin time (APTT).

The relationship between right ventricular lead position and paced QRS duration.

BACKGROUND: The relationship between the anatomical location of right ventricular pacing site and paced QRS duration is unclear. In this study, we aimed to investigate the relationship between right ventricular pacing site and paced QRS duration using cardiac angiography. METHODS: Fifty patients were implanted with pacemakers. The right ventricular lead position was determined from the findings of cardiac angiography and the paced QRS duration was measured. Cardiac angiography was used to display the right ventriculogram (RVG) and the left ventriculogram (LVG). The RVG view was divided into three areas and the LVG view was divided into four areas. RESULTS: The paced QRS duration value was significantly longer in the right ventricular apex area compared with the outflow and inflow areas (160 ± 15 ms vs 140 ± 15 ms, P = 0.02, and vs 133 ± 17 ms, P < 0.001, respectively), but those values were not statistically significantly different between the right ventricular outflow and the right ventricular inflow areas (140 ± 15 ms vs 133 ± 17 ms, P = 0.187). When assessed with LVG views, there were the statistically significant differences in the paced QRS duration values in all areas except the apex area. (LV mid-anterior: 147 ± 11 ms vs LV base: 127 ± 13 ms, P < 0.001, and vs LV mid-septum: 129 ± 12 ms, P = 0.001, respectively.) CONCLUSIONS: Cardiac angiography showed that there was a relationship between the anatomical right ventricular pacing site and paced QRS duration. Cardiac angiography can help determine the areas that produce shorter paced QRS duration.

Left ventricular remodeling after myocardial infarction impairs early diastolic, but not systolic, function in the radial direction in the remote normal region.

BACKGROUND: It is acknowledged that expansion of the remote normal region of the left ventricle causes remodeling after myocardial infarction (MI). However, the characteristics of that region have not been fully elucidated. METHODS: We studied 13 patients with atypical chest pain (controls) and 15 patients with a prior anterior MI who underwent cardiac catheterization. With Doppler strain imaging, we measured the peak radial myocardial systolic strain and peak radial early diastolic strain rate at the posterior wall of the left ventricle. None of the patients with atypical chest pain exhibited significant stenosis of the three major coronary arteries or left ventricular (LV) wall motion abnormality in cardiac catheterization. The patients with a prior anterior MI had single anterior descending artery disease without wall motion abnormality in the LV inferoposterior wall. LV ejection fraction and the LV relaxation time constant were also measured. RESULTS: The LV ejection fraction was significantly smaller in patients with a prior MI compared to controls. The peak radial systolic strain in the LV posterior wall was not significantly different between the patients with a prior MI and controls (125 ± 49 vs. 122 ± 29%). In contrast, the peak radial early diastolic strain rate in the same area was significantly lower in the patients with a prior MI than in controls (-7.4 ± 2.7 vs. -13.2 ± 4.0 s(-1), p < 0.001). Peak early diastolic radial strain rate was significantly correlated with the LV relaxation time constant in all patients (r = 0.69, p < 0.001). CONCLUSION: LV remodeling after an MI impairs local early diastolic myocardial function in the remote normal region and it is related to global LV diastolic dysfunction.