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The single-lead VDD pacemaker system (VDDPS) enables atrial synchronous ventricular pacing with only one lead in patients with an atrioventricular block. There are some cases in which the atrial potential decreases after implantation of a VDDPS, making physiological pacing difficult. The mechanism of this decrease has not been elucidated yet. To elucidate the possible relationship between the decrease of the atrial potential after implantation of a VDDPS and histopathological changes of the atrium. We implanted a VDDPS from the jugular vein under anesthesia in 10 adult dogs. The tip of the pacing lead was fixed in the right ventricular apex of the heart under fluoroscopic guidance. Then, the lead was ligated and fixed to the jugular vein at a point where a favorable atrial potential was obtained. The end of the lead was passed from the neck to the back subcutaneously; then pulled outside and fixed there to measure the atrial potential. The atrial potential was measured using a pacing system analyzer under anesthesia on days 3 (n = 9) and 7 (n = 8), as well as on weeks 2 (n = 6), 3 (n = 4), and 4 (n = 3), after the implantation. The heart was removed from the dogs on day 3 (n = 2), day 7 (n = 2), week 2 (n = 2), and week 4 (n = 4) to examine the atrial histological findings. The atrial potential was 2.7 +/- 0.7 mV at the time of the implantation, 1.7 +/- 1.1 mV (P < 0.05) on day 3, and 1.7 +/- 0.7 mV on week 4 after the implantation. Macroscopically, the pacemaker lead was covered with thrombus, and adhered to the atrial wall in 80% of animals. Microscopically, the endocardium was hypertrophic due to fibrous tissue; besides RBC extravasation, inflammatory cells infiltration and degeneration of myocardial cells, were observed under the endocardium. Inflammatory changes developed in the atrial wall after implantation of the VDDPS, and this seemed to be one of the mechanisms for the decrease of the atrial potential of the VDDPS.

Background Left atrial ( LA ) dilation is associated with morbidity of atrial fibrillation ( AF ). However, little is known about pulmonary vein ( PV ) dilation. Purpose We investigated the PV volume in the patients with AF . Methods and results We performed 3dimensional computed tomography (3D CT ) in 155 patients and divided them into three groups: 19 patients without AF (non‐ AF group, mean age 66 ± 12 years), 50 with paroxysmal AF ( PAF group, mean age 67 ± 8 years) and 24 with persistent AF (Pe AF group, mean age 64 ± 10 years). The absence of AF was diagnosed in patients with a cardiac implantable electronic device for at least 1 year (mean: 59 ± 37 months). We determined the PV volume as the total volume from the orifice to the first branch of each PV . According to the echocardiographic data, the LA dimension ( LAD ) and LA volume index ( LAVI ) were largest in the Pe AF group followed by the PAF and non‐ AF group. According to the morphometric data obtained on 3D‐ CT , the PV volume was similar in Pe AF and PAF groups but significantly smaller in the non‐ AF group (median value: 24 vs 21 vs 14 mL, respectively). According to the receiver operating characteristic curve analysis, the area under the curve for the PV volume in the presence of AF was 0.80, and the optimum cut‐off value was 17 mL (sensitivity 74%, specificity 80%). Conclusion The PV volume might be useful for predicting the presence of AF before increases in the LAD and LAVI on echocardiography.

ICE imaging of the LA-PV junction permitted real time monitoring of the target sites for PVI during the ablation procedure, and was considered a useful technique for performing PVI.

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A 52-year-old woman with intermittent complete atrioventricular (AV) block detected on exercise was admitted to the hospital. Echocardiography revealed lesions on the right ventricular side of the interventricular septum and free wall of the basal inferolateral area. Gadolinium-enhanced cardiovascular magnetic resonance (CMR) imaging revealed the mass and wall thickening at the same locations with late gadolinium enhancement (LGE). Focal uptake at the septal lesion was detected using 67Ga scintigraphy. Focal on diffuse intense uptake in the lesions was observed on Fluorine-18 fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) imaging. Whole-body CT and laboratory evaluations uncovered no signs of malignant tumors in other organs. Ophthalmologic evaluation revealed ophthalmologic sarcoidosis. Although the result of endomyocardial biopsy was negative, the presence of cardiac sarcoidosis was strongly suggested on the basis of the new Japanese guidelines published in 2017. AV conduction disturbance and tracer accumulation on 67Ga scintigraphy completely disappeared after 2 weeks of steroid therapy. The size of mass, inferolateral wall thickness in echocardiography and CMR, and standardized uptake value (SUV) of the masses on 18F-FDG PET also decreased over time.

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M ultiple coronary fistulae that drain into the left ventricle are rarely associated with apical hypertrophic cardiomyopathy.1 On the other hand, associations of left ventricular noncompaction (LVNC) and multiple coronary fistulae or hypertrophic cardiomyopathy have previously been reported in several cases. 2,3 We report here a unique case of apical hypertrophy of the left ventricle, multiple coronary-left ventricular fistulae, and a morphological structure of the left ventricular myocardium mimicking LVNC. Case PresentationA 59-year-old man was admitted to our hospital for fever and rapidly progressing dyspnea that had persisted for 10 days. He had been diagnosed with apical hypertrophic cardiomyopathy in his 30s, although he had no regular medical checkups and was asymptomatic. On admission, the patient had mild wheezes audible in the midportion of the right lung and a diastolic murmur heard at the Erb and the cardiac apical area.Chest x-ray and computed tomography revealed cardiac enlargement with increased pulmonary vasculature, granular shadows in the lower areas of both lungs, and increased density of the right middle lung area. These findings suggested failure of the left side of the heart with pneumonia. A 12-lead electrocardiogram (ECG) confirmed normal sinus rhythm with inverted T waves in leads II, III, aVF, and V 3 through V 6 (Figure 1). He recovered rapidly with antibiotics and standard therapy for heart failure.Transthoracic 2-dimensional echocardiography showed diffuse hypertrophy of the mid to apical left ventricular walls ( Figure 2A and Movie I in the online-only Data Supplement). Doppler echocardiography revealed multiple areas of mosaic color flow within the anterior, lateral, and apical myocardium connected to the left ventricular cavity, with a peak flow speed of 0.8 to 0.9 m/s in the diastolic phase ( Figure 2B and Movie II in the online-only Data Supplement). Enlarged left and right coronary arteries and rapid diastolic flow with a peak speed of 1.5 m/s in the left anterior descending artery were also identified.A markedly enlarged, tortuous coronary artery with multiple coronary artery-left ventricular fistulae was visible on cardiac computed tomography examination ( Figure 3A). Coronary computed tomography angiography, diastolic-phase imaging, showed a 2-layer left ventricular myocardium mimicking LVNC, with a maximal ratio of noncompacted to compacted myocardium of 2.2 ( Figure 3B and 3C).Coronary angiography confirmed multiple fistulae between the left and right coronary arteries and the left ventricle ( Figure 4A and 4B). Left ventricular angiography revealed a spade-shaped cavity indicative of apical hypertrophic cardiomyopathy.Cine magnetic resonance images showed small fine trabeculae extending from the lower base to the apical anterior, lateral, and inferior endocardium in the diastolic phase. In the systolic phase, thickening of both layers of the myocardium (mimicking compacted and noncompacted myocardium) was present (Movies III and IV in the online-only Data Supplement). Di...