Endovascular Embolization of Coronary Artery-Pulmonary Artery Fistulas with Double Coronary Aneurysms.

A 75-year-old woman with chest discomfort and a continuous murmur was admitted to our hospital. During noninvasive examination, computed tomography angiography showed a coronary artery-pulmonary artery fistula with double giant coronary aneurysms (one was 42 mm× 32 mm× 32 mm, and the other was 25 mm× 20 mm× 17 mm) arising from the proximal part of the left anterior descending (LAD) artery. Stress myocardial scintigraphy showed ischemia at the LAD area. Given her frailty, the heart team, including cardiac surgeons, judged that surgical treatment would be difficult. Thus, endovascular embolization for the abnormal vessels was selected. After coronary angiography, two coronary aneurysms were embolized by 53 coils, and the feeding artery was embolized by two coils and one Amplatzer Vascular Plug 4™. A small pulmonary artery fistula remained after the procedures; thus, additional embolization was performed 3 months after the index procedure. Thereafter, angiography showed no flow into the aneurysms, and her symptoms improved.Endovascular embolization might be an effective treatment to achieve aneurysm occlusion in patients at high risk for surgical treatment. Although the present case had double coronary aneurysms with a large feeder vessel, the combination procedure of coils and vascular plug was able to embolize this abnormal vessel.

A case report of stomach perforation during automatic mechanical chest compression following pulseless electrical activity due to cibenzoline intoxication.

BACKGROUND: The current report describes a case of stomach perforation, a rare but serious complication, that occurred during cardiopulmonary resuscitation following severe cibenzoline intoxication. CASE PRESENTATION: A woman aged in her 30s was brought into our hospital while receiving cardiopulmonary resuscitation for pulseless electrical activity. After starting extracorporeal membrane oxygenation (ECMO), her abdominal X-ray examination revealed free air in her abdomen. She was diagnosed with internal gastric perforation. An emergency operation was carried out while the circulation was maintained using ECMO. As the patient's blood cibenzoline concentration on admission was 3,868 ng/mL, she was diagnosed with cibenzoline intoxication caused by the self-intake of twice the prescribed dose. She was successfully weaned off ECMO and discharged alive with full recovery. CONCLUSION: We successfully treated a case of gastric perforation after pulseless electrical activity requiring ECMO support due to cibenzoline intoxication. Abdominal surgery can be carried out even if ECMO support is needed.

CHADS2 and modified CHA2DS2-VASc scores for the prediction of congestive heart failure in patients with nonvalvular atrial fibrillation.

BACKGROUND & PURPOSE: We have conducted a retrospective observational study to analyze the correlation between the CHADS2 score, the modified CHA2DS2-VASc (mCHA2DS2-VASc) score, and the incidence of all-cause death and congestive heart failure (CHF). METHODS: The study cohort consisted of 292 consecutive patients with nonvalvular atrial fibrillation (NVAF) admitted to our hospital from 2012 to 2014. Electronic medical records were used to confirm medical history including prior heart failure, hypertension, diabetes, stroke, and coronary disease. A follow-up survey for all-cause deaths and incidence of CHF was carried out from the baseline data to May 2015. We analyzed the correlation between each score and the endpoints using the Kaplan-Meier method and the Cox proportional hazards model. RESULT: During the follow up period (mean=1.6 years), 69 all-cause deaths and 58 CHF events occurred in the cohort. There was no significant association between these scores and all-cause death in our CHF cohort. The incidence of CHF significantly increased along with increased CHADS2 (p=0.018) or mCHA2DS2-VASc scores (p=0.044). The hazard ratio (HR) for CHF after adjustment for drug treatment was obtained from a Cox proportional hazards model. The HRs for the CHADS2 and mCHA2DS2-VASc scores were 1.38 (95% CI; 1.13-1.68) and 1.35 (95% CI; 1.24-1.59), respectively. CONCLUSION: Calculation of the CHADS2 and mCHA2DS2-VASc scores in order to evaluate the risk of systemic thromboembolism was useful to predict the onset of CHF, but not all-cause death, in patients with NVAF.

Increased carotid artery stiffness without atherosclerotic change in patients with aortic dissection.

The arterial properties and pathogenesis of aortic dissection remain obscure. To examine the arterial properties of patients with aortic dissection, the authors studied the ultrasonographic characteristics of the carotid artery in patients with an aortic dissection (AD, n = 86), and compared these findings with data of patients suffering from arteriosclerosis obliterans (ASO, n = 151), coronary artery disease (CAD, n = 163), and with healthy controls (HC, n = 77). Atherosclerotic intimal changes, such as intima-media thickness (IMT) and plaque formation, were milder in AD than in ASO or CAD (IMT: 0.83 +/- 0.16 vs 0.93 +/- 0.20/0.86 +/- 0.17 mm, p < 0.05; plaque number: 0.6 +/- 1.1 vs 2.7 +/- 2.4/2.5 +/- 2.1, p <0.05). Luminal diameter in AD, ASO, and CAD was significantly higher than in HC. The luminal distensibility in AD was decreased compared with HC but was the same as in ASO and CAD. Intra-AD group analysis showed that in patients with an intramural hematoma (IMH) or a dissection with a thrombosed false lumen (TLF) the IMT was higher than in patients with a classic dissection. In addition, plaque formation was more severe in AD patients with a coexisting abdominal aortic aneurysm (AAA). Reduced distensibility without severe intimal disease was found in AD. These findings suggest that patients with AD may have several arterial alterations, including structural abnormalities. Patients with IMH, TFL, or coexisting AAA may differ from patients who have a classic type of dissection or who do not have AAA, in terms of arterial characteristics including intimal disease and wall elastic property, and the initiating cause of the dissection.

Peripheral vasodilatory dysfunction in adult patients with congenital heart disease and severely elevated pulmonary vascular resistance.

Several studies have demonstrated that pulmonary vascular abnormalities precede alterations in aortic circulation downstream in animal models of heart failure. The relationship between increased pulmonary vascular resistance (PVR) and agonist-induced limb vasodilatory response remains unknown in patients with congenital cardiovascular shunt lesions (CSL). The authors hypothesized that patients with CSL and severely elevated PVR will show a defective vasomotor response in the peripheral vascular bed. To examine this hypothesis we measured forearm blood flow (FBF) responses to the endothelium-dependent vasodilator acetylcholine and the endothelium-independent vasodilator sodium nitroprusside. The values for these FBF responses were compared with PVR in adult patients with CSL (n=20) and healthy age- and sex-matched controls (n = 15). When patients with CSL were divided into 2 subgroups by median value of PVR, in the lower PVR subgroup, acetylcholine-induced FBF changes were selectively and significantly lower than in the healthy control group (p <0.05). In the higher PVR subgroup, FBF responses to both acetylcholine and sodium nitroprusside were significantly blunted compared to healthy controls (both p < 0.01). In addition, when FBF changes above baseline for each dose of acetylcholine and sodium nitroprusside were cumulated and used as acetylcholine response and sodium nitroprusside response, the sensitivity and specificity for identifying patients with Eisenmenger's type of CSL was 100% and 80% by acetylcholine response, and 67% and 80% by sodium nitroprusside response, respectively. In conclusion, adult CSL patients with elevated PVR and severe pulmonary arterial hypertension showed generalized vasodilator dysfunction in the forearm vasculature. This result suggests that upper limb resistance vessel dysfunction may be an indicator for advanced stage of adult patients with CSL.

Population-based incidence of sudden cardiac and unexpected death before and after the 2011 earthquake and tsunami in Iwate, northeast Japan.

BACKGROUND: The aim of this study was to evaluate the temporal impact of the 2011 Japan earthquake and tsunami on the incidence of sudden cardiac and unexpected death (SCUD). METHODS AND RESULTS: We surveyed the impact of the disaster on the incidence and clinical characteristics of SCUD in Iwate. To perform complete identification of SCUD for 8 weeks before and 40 weeks after the disaster, medical records and death certificates relevant to SCUD were surveyed in the study area. Compared with the previous year's rate, the incidence (per 10 000 person-year) of SCUD for the initial 4 weeks after the disaster (acute phase) was double (33.5 vs 18.9), and thereafter the rate returned to the previous level. Significant relationships were found between weekly numbers of SCUD and seismic activity (intensity, r=0.43; P<0.005: frequency, r=0.46; P<0.002). The standardized incidence ratio (SIR) of SCUD in the acute phase was significantly increased compared with that of previous years (1.71, 95% CI 1.33 to 2.16). Increased SIRs were predominantly found in female subjects (1.73, 95% CI 1.22 to 2.37), the elderly (1.73, 95% CI 1.29 to 2.27), and residents living in the tsunami-stricken area (1.83, 95% CI 1.33 to 2.46). In addition, SIRs for weekdays (1.71, 95% CI 1.28 to 2.24) and nights-mornings (2.09, 95% CI 1.48 to 2.86) were amplified. CONCLUSIONS: The present results suggest that the magnitude of a disaster, related stress, and population aging may cause a temporary increase in the incidence of SCUD with amplification of ordinary weekly and circadian variations.

Left coronary artery ostial stenosis from Takayasu's arteritis diagnosed using transthoracic color flow and pulsed Doppler echocardiography.

Coronary artery stenosis is seen in 10-45% of patients with Takayasu's arteritis (TA) and coronary ostia are most frequently involved. It may cause angina pectoris and sudden death during the early course of the disease. We describe a 14-year-old girl who first presented with exertional angina and syncope and was diagnosed as having left coronary artery ostial stenosis from TA by using transthoracic echocardiography. This is the first report showing the important role of color flow and pulsed Doppler echocardiography to detect coronary artery stenosis caused by TA.

Nitric oxide plays an insignificant role in direct vasodilator effects of calcium channel blockers in healthy humans.

Several experimental studies have suggested that the vasodilatory effects of calcium channel blockers (CCBs) are due in part to an endothelium-dependent mechanism. However, it remains unknown whether CCBs directly augment liberation of endothelium-derived dilator substances such as nitric oxide (NO) in the human vasculature. The aim of this study was to examine whether CCBs of several kinds directly increase the bioavailability of NO in forearm resistance vessels. Twenty-four healthy men (mean age 30 +/- 2 years) were randomly assigned to three study groups (n = 8 in each), and each group was assigned one of three first-generation CCBs (nifedipine, nicardipine, diltiazem). Subdepressor doses of CCBs [4, 8, 16, 24, and 36 (diltiazem only) nmol/min; for 2 min in each dose] were infused intra-arterially, and forearm blood flow (FBF) was determined plethysmographically. After control FBF responses to CCBs had been measured, a NO synthase inhibitor (N(G)-monomethyl-L-arginine: L-NMMA) was infused intra-arterially, and the FBF response to CCBs was again determined. Further, as a positive control for NO stimulation, acetylcholine (ACh) was also examined before and after L-NMMA in each group. Systemic blood pressure and heart rate did not change significantly during the study protocol. The FBF responses to these CCBs did not differ before and after NO synthase inhibition by L-NMMA (FBF at maximum doses: nifedipine, 8.0 +/- 0.8 vs. 7.3 +/- 0.7; nicardipine, 7.3 +/- 1.5 vs. 6.5 +/- 1.3; diltiazem, 5.7 +/- 0.7 vs. 4.2 +/- 0.7 ml/min per 100 ml: all not significant), although FBF responses to ACh were significantly reduced by L-NMMA. In conclusion, direct NO liberation does not make a significant contribution to the vasodilation associated with first-generation CCBs in healthy human resistance vessels.