A pacemaker-induced venous obstruction is relatively common, but is rare in cases where chronic venous occlusion has developed and progressed after the removal of permanent pacemaker leads. We report a case of permanent pacemaker implantation following percutaneous balloon venoplasty in a patient with innominate vein stenosis. The patient had a history of permanent pacemaker implantation, using a right subclavian approach, with lead extraction due to infective endocarditis 6 years earlier. Although the epicardial leads were re-implanted, once more the ventricular lead broke. When we tried to implant a new pacemaker, using a left subclavian endovascular approach, extensive venous stenoses of the innominate, right internal jugular and subclavian veins were found. As it was impossible to advance the standard pacemaker lead; therefore, percutaneous balloon venoplasty of the innominate vein was performed, and a DDD-R pacemaker successfully implanted.
Angioplasty, Balloon ; Brachiocephalic Veins* ; Constriction, Pathologic* ; Endocarditis ; Humans ; Pacemaker, Artificial ; Subclavian Vein ; Venous Thrombosis

No abstract available.
Atrial Fibrillation ; Risk Factors

BACKGROUND: Myocardial contrast two-dimensional echocardiography(MC-2DE) has been known to have the real time capabilities for repeat in vivo assessment of ischemic risk areas and for evaluation of the myocardial perfusion. The aims of this investigation are (1) to evaluate the feasibility of MC-2DE for the delineation and quantitation of the area at risk. (2) to determine the relationship between the extent of the echocontrast defect area(EDA) during reperfusion and the size of myocardial infarction as determined by post-mortem tissue examination, and (3) to observe serial changes in the time echo-intensity characteristics of MC-2DE during coronary occlusion and reperfusion. METHODS: Myocardial contrast echocardiographic images were made by injecting bolus 5mL of two-syringe-agitated mixture of sodium meglumine ioxaglate(Hexabrix(R)) and normal saline(2 : 3 by volume) into the aortic root before and during coronary occlusion of the left anterior descending coronary artery, distal to the first diagonal branch and during reperfusion on eight open-chest dogs. Two-dimensional echocardiographic short axis views were obtained at four anatomic levels : the apex, the low papillary muscle, the high papillary muscle and the mitral valve. The changes in EDA and echo-intensity with its wash-out half time(WHT) at the high papillary muscle level during coronary occlusion and reperfusion were measured every 15 minutes. The total EDA was measured by planimetry at 3 minutes after coronary occlusion and at 60 minutes after reperfusion. Evans blue or methylene blue were used for the measurement of the anatomic area at risk and triphenyl-tetrazolium chloride(TTC) for the measurement of the infarct area. RESULTS: The EDA measured 30 minutes after coronary occlusion(19.6%) was smaller than that at 3 minutes after coronary occlusion(24.0%, p<0.01). Then EDA at 3 minutes occlusion was strongly predictive of the anatomic extent of area at risk(EDA=0.48 Area at risk+16.95, r=0.84, p<0.05). The EDA at 60 minutes after reperfusion, which showed an irregular margin and was located within the subendocardium of the area at risk, also correlated well with the infarct area(IA)(EDA=0.78 IA+3.32, r=0.82, p=0.09). The peak echo-intensity in the ischemic area during coronary occlusion was significantly low(14.2+/-6.5 vs 73.8+/-31.7 in the non-ischemic area, p<0.01) and the WHT was delayed more in the ischemic area than in the non-ischemic area(23.2+/-2.8 sec vs 8.1+/-3.3sec, p<0.01). During the period of reperfusion, WHT in the previously ischemic area was markedly delayed compared to that in the non-ischemic area (p<0.01), although the peak echo-intensity in the ischemic area at 3 minutes after reperfusion increased modestly compared to that in the non-ischemic area(80.9+/-22.8 vs 72.7+/-8.4), suggesting the impairment in the transit of microbubbles is probably due to microvascular damage after reperfusion. There were no adverse hemodynamic or electrocardiographic effects after injection of the contrast agent. CONCLUSIONS: These findings suggest that myocardial contrast echocardiography was useful as a non-invasive technique, first, to delineate the area at risk in vivo during coronary occlusion and, after reperfusion, the infarct area, and secondly, to evaluate indirectly the state of myocardial perfusion during coronary occlusion and reperfusion.
Animals ; Axis, Cervical Vertebra ; Coronary Occlusion* ; Coronary Vessels ; Dogs ; Echocardiography* ; Electrocardiography ; Evans Blue ; Hemodynamics ; Meglumine ; Methylene Blue ; Microbubbles ; Mitral Valve ; Myocardial Infarction ; Papillary Muscles ; Perfusion* ; Reperfusion* ; Sodium

No abstract available.
Anticoagulants ; Atrial Fibrillation ; Humans

Background and Objectives: Cryoballoon catheter ablation for the treatment of patients with symptomatic atrial fibrillation (AF) has been adopted globally, but there are limited multicenter reports of 12-month outcomes in the Korean patient population. This analysis evaluated the clinical performance and safety of cryoballoon ablation (CBA) according to standard-of-care practices in Korea. Methods: This evaluation of Korean patients with AF was conducted within the larger Cryo Global Registry, which is a prospective, multicenter, post-market registry. Freedom from a ≥30-second recurrence of atrial arrhythmias (after a 90-day blanking period until 12 months) and procedural safety were examined in subjects treated with CBA at 3 Korean centers. Results: Overall, 299 patients with AF (60±11 years old, 24.7% female, 50.5% paroxysmal AF) underwent CBA using the Arctic Front Advance cryoballoon. Of those, 298 were followed-up for at least 12 months. Mean procedure-, left atrial dwell- and fluoroscopy time was 76±21 minutes, 56±23 minutes, and 27±23 minutes, respectively. Freedom from AF recurrence at 12 months was 83.9% (95% confidence interval [CI], 76.9–88.9%) in the paroxysmal and 61.6% (95% CI, 53.1–69.0%) in the persistent AF cohort. Rhythm monitoring was performed on average 4.7±1.4 times during the follow-up period. Serious device- or procedure-related adverse events occurred in 2 patients (0.7%). The 12-month Kaplan-Meier estimate of freedom from repeat ablation and cardiovascular-related hospitalization was 93.8% (95% CI, 90.4–96.1%) and 89.7% (95% CI, 85.6–92.7%), respectively. Conclusions CBA is an efficient, effective, and safe procedure for the treatment of AF patients when used according to real-world practices in Korea.Trial Registration: ClinicalTrials.gov Identifier: NCT02752737

BACKGROUND AND PURPOSE: Left ventricular hypertrophy (LVH) is a well known cardiovascular risk factor, independent of hypertension, even in the absence of epicardial coronary artery disease. Possible mechanisms have been proposed, including increased LV mass, reduced coronary flow reserve (CFR) and diastolic filling abnormalities. However, the relations among LV hypertrophy, diastolic function, hypertension and coronary flow reserve (CFR) in patients with chest pain and normal coronary angiograms have not been well defined. SUBJECTS AND METHOD: Twenty-six patients with chest pain and normal coronary angiograms were included. LV mass, isovolumic relaxation time (IVRT), deceleration time (DT) and E/A ratio were assessed by 2-D echo-cardiography. Coronary blood flow velocity before and after intracoronary adenosine were measured using intracoronary Doppler wire (FIoWire). CFR was defined as ratio of peak flow velocity after adenosine to baseline flow velocity. Subjects were devided into 4 groups according to presence of LVH and hypertension and the parameters were compared among groups. RESULTS: FR was lower (p<0.01) in the groups with either hypertension or LVH or both than in the groups without them. The decrement in CFR was not linearly related to the degree of LVH (r=0.31, p=0.135). Although there were modest increment in IVRT and DT and decrement in E/A ratio in the groups with hypertension or LVH or both, there was no statistical significance. CONCLUSION: These findings suggest that the underlying mechanism of impaired CFR in patients with LVH or hypertension may be the consequence of primary coronary microvascular lesion rather than the process of left ventricular hypertrophy.
Adenosine ; Blood Flow Velocity ; Chest Pain* ; Coronary Artery Disease ; Deceleration ; Humans ; Hypertension ; Hypertrophy ; Hypertrophy, Left Ventricular ; Relaxation ; Risk Factors ; Thorax*