RESUMEN
Transvenous pacemaker leads may impair tricuspid valve coaptation, and is a well-known cause of tricuspid regurgitation (TR). The mechanism underlying TR may be the perforation or laceration of the valve leaflets, direct lead interference with the valve closure, or adhesion of scar tissue between the leads of the pacemaker and the valve leaflet. Recently, three-dimensional echocardiography has clarified the pathway of the pacing lead and its interference with the tricuspid valve, but surgical treatment is not conventionally performed in the early stages of TR because of the necessity of the pacing lead. Occasionally, patients with TR develop severe right-sided heart failure, and the operative mortality in such conditions is very high. Thus, it is important to study the relationship between transvenous leads and TR. Tricuspid valve surgery is usually performed after replacing the transvenous lead with an epicardial lead. However removal of the transvenous lead may cause injury to the right ventricle, and ventricular chronic stimulation thresholds with epicardial stimulation have been shown to be significantly higher than those with endocardial stimulation. We performed TR surgery in 5 patients without removing the transvenous leads. To avoid interference with the valve closure, we shifted the pacemaker leads to the commissure and fixed them to the annulus. All the patients underwent successful tricuspid valve repair or replacement, and the symptoms of right-sided heart failure improved after the operation. We concluded that this technique is a very simple, and feasible method for treatment of most patients with TR caused by pacing leads.
RESUMEN
A 75-year-old man was admitted to our hospital because of severe aortic stenosis associated with fainting spells. He had undergone coronary artery bypass grafting at the age of 66, and had progressive aortic stenosis for 9 years. Ultrasound showed left ventricular hypertrophy and a calcified aortic valve. The aortic valve area was 0.34 cm<sup>2</sup> and the mean pressure gradient was 56 mmHg. Multi detector-row computed tomography showed patent bypass grafts (LITA-LAD, SVG-OM-PL, and SVG-RCA) and a persistent left superior vena cava (PLSVC). Coronary angiography revealed total occlusion of all the 3 native coronary arteries, therefore, antegrade cardioplegic perfusion was impossible. Retrograde perfusion was also impossible because of the PLSVC. We had to clamp the LITA and infuse the cardioplegic solution through the SVG graft to obtain cardioplegic arrest. Performing aortic valve replacement (AVR) on a beating heart facilitates the operation, because it negates the need to clamp the patent bypass graft and the PLSVC. We exposed a minimal area of the operating field, ascending aorta, and right atrium. Cardiopulmonary bypass was established by cannulating the ascending aorta and right atrium. The right pulmonary vein was cannulated for left ventricular venting. The ascending aorta was cross clamped on the proximal side of the SVG. AVR was thus performed using the standard approach on the beating heart with coronary perfusion through the bypassed graft. The postoperative course was uneventful, and the patient was discharged 15 days postoperatively. Redo surgery is more complex than primary surgery and is associated with higher mortality and morbidity. Beating heart surgery is one of the optional methods in such a complex case.
RESUMEN
For patients with advanced heart failure, surgical left ventricular restoration (SVR) is an option usually evaluated by nuclear cardiac imaging, magnetic resonance imaging and ultrasonography. The clinical application of multi detector-row computed tomography (MDCT) has been increasingly extended to evaluate not only coronary artery stenosis, but also cardiac function, myocardial perfusion and viability. We report a successful surgical case of ischemic cardiomyopathy evaluated by MDCT in pre- and post-LVR. A 59-year old man was admitted to our hospital because of worsening heart failure. He had a history of coronary artery bypass grafting after myocardial infarction of the anterior wall at age 45 but had discontinued his medication 5 years previously. Ultrasonography showed poor left ventricular function, massive mitral regurgitation and a floating mural thrombus which required emergency surgery. In addition to conventional coronary angiography, electrographically-gated MDCT clearly described the complex coronary anatomy and stenosis, global and regional left ventricular function, and the relation between the mural thrombus and the scarred myocardium. Thrombectomy, LVR (overlapping type), coronary artery bypass grafting and mitral annuloplasty were performed. Postoperative MDCT showed improvement in left ventricular volume and function in the time-volume analysis, in wall thickness and wall thickening in both the SVR site and remote sites in four-dimensional volumetric imaing. Our case suggests that MDCT can be a valuable tool for the cardiac surgeon.