Phos-tag There are many instances of angiectopia other than

There are many instances of angiectopia other than those associated with scoliosis. For example, anomalies and variations of inferior vena cava anatomy without abnormal cardiac comorbidity occur in approximately 0.3% of the population, depending on the specific abnormality [4]; however, these anatomical variations are often clinically silent and incidentally discovered. Venous CT images, particularly in cases that are anatomically different, ensure appropriate localization of the vein and heart. Prior CT is very effective to avoid discovering unexpected anatomical differences during ablation. Therefore, not only 3D CT reconstruction of the LA and pulmonary vein, but also venous CT images, is important in AF ablation with complex Phos-tag and vein morphology.
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Introduction A sigmoid-shaped interventricular septum (SIS) is generally considered a normal part of the aging process and is of little clinical significance. However, certain patients with SIS may experience clinical symptoms such as dyspnea upon effort and syncope. In patients with hypertrophic obstructive cardiomyopathy (HOCM), narrowing of the left ventricular outflow tract (LVOT) generates a left ventricular (LV) pressure gradient, resulting in reduced cardiac output and subsequent syncope. In these patients, the vasovagal reflex, i.e., the Bezold–Jarisch reflex [1], could play an important role in the occurrence of syncope. By contrast, the mechanisms of syncope in patients with SIS without left ventricular hypertrophy (LVH) [2–4] have yet to be fully elucidated. Here, we report two patients with SIS who presented with recurrent syncope. We were successful in clarifying the mechanisms of syncope and effects of beta-blockers in these cases.
Case 1 An 81-year-old man with no history of heart disease was admitted to our hospital for the treatment of recurrent episodes of syncope after drinking. He experienced the first episode at age 75. On admission, his blood pressure (BP) was 144/81mmHg and the heart rate (HR) was 56beats/min. Physical examination was otherwise unremarkable except for a grade 2/6 systolic ejection murmur at the apex area. Routine blood tests were unremarkable. A chest X-ray revealed a cardiothoracic ratio of 51%. A 12-lead electrocardiogram revealed normal sinus rhythm and left axis deviation without LVH, ST segment depression, and T-wave inversion. Two-dimensional transthoracic echocardiography (2DE) revealed an SIS protruding into the LV (Fig. 1A) and normal systolic function (ejection fraction, 77%). LVH was not evident (interventricular septum/posterior wall=8/8mm). Color Doppler echocardiography revealed turbulent systolic flow at the LVOT with a pressure gradient of 8mmHg, determined by continuous-wave Doppler (Fig. 1B). The reliability of the Doppler measurement of the pressure gradient at the LVOT was validated by a board certified fellow of the Japan Society of Ultrasonics in Medicine (JSUM). M-mode echocardiography demonstrated systolic anterior movement of the mitral chordae tendineae. To investigate the cause of syncope after drinking, a head-up tilt test (HUT) was performed with 25g of alcohol loading. At 16min of a 60-degree HUT, the LVOT pressure gradient increased from 8 to 176mmHg, and M-mode echocardiography demonstrated mid-systolic hemiclosure of the aortic valve that was not noted when the patient was in the supine position (Fig. 1C). At 18min of HUT, the patient experienced presyncopal symptoms with a decrease in both BP and HR (from 138/74 to 83/46mmHg and from 52 to 46 beats/min, respectively). HUT with 0.3mg nitroglycerine (NG) provocation (HUT+NG) also induced hypotension and bradycardia with presyncopal symptoms following an increase in the LVOT pressure gradient. We started the patient on bisoprolol (2.5mg/day), and his syncopal episodes have not recurred since.
Case 2 A 66-year-old man presented with recurrent syncope after drinking. On admission, his BP and HR were 123/82mmHg and 65beats/min, respectively. Physical examination was unremarkable except for a grade 2/6 systolic ejection murmur at the fourth intercostal space on the left sternal border. An electrocardiogram revealed sinus rhythm (62beats/min) and left axis deviation without LVH and ST-T changes. His chest X-ray was normal, and 2DE showed SIS with normal systolic function (ejection fraction, 74%). LVH was not evident (interventricular septum/posterior wall=6/6mm). Color Doppler echocardiography revealed turbulent systolic flow at the LVOT with a peak pressure gradient of 8mmHg, determined by continuous-wave Doppler. M-mode echocardiography demonstrated systolic anterior movement of the mitral chordae tendineae. After excluding other possible causes of syncope with non-invasive tests, HUT was performed (Fig. 2). No symptoms occurred, and both BP and HR were not significantly decreased during the baseline tilt (60°) or during HUT+NG. However, presyncopal symptoms developed in association with abrupt hypotension and baradycardia at 2.5min of HUT with an isoproterenol infusion (0.015µg/kg/min). A Task Force Monitor® (CN Systems, Graz, Austria) revealed that at the time of presyncope, total peripheral vascular resistance (TPR) decreased (Fig. 2) and high-frequency power increased (Fig. 3). Therefore, a diagnosis of vasovagal reflex was made based on the HUT with an isoproterenol infusion. An isoproterenol provocation test was also performed in the supine position. At 1min and 46s after initiating the isoproterenol infusion (0.02µg/kg/min), hypotension and sinus bradycardia were induced along with ventricular escape beats and presyncopal symptoms (Fig. 4). At that time, the peak pressure gradient at the LVOT was increased from 8 to 59mmHg with a decrease in TPR. We started the patient on bisoprolol (2.5mg/day), and his syncopal episodes have not recurred since.