Effects of azilsartan compared to other angiotensin receptor blockers on left ventricular hypertrophy and the sympathetic nervous system in hemodialysis patients.

Hypertension is a major risk factor for cardiovascular and cerebrovascular events, and most patients with hypertension are administered antihypertensive drugs. However, not all patients achieve normal blood pressure levels. The new angiotensin receptor blocker azilsartan (Takeda Pharmaceutical Company Limited, Osaka, Japan) has been reported to have a strong hypotensive effect. Our study investigated the efficacy of azilsartan compared with other angiotensin receptor blockers. This study included 17 hypertensive patients on HD, who had been administered angiotensin receptor blockers, except for azilsartan, for more than 6 months before enrolling, and after enrollment, they were switched to azilsartan. Blood tests, Holter electrocardiogram, ambulatory blood pressure monitoring, and echocardiography were performed at baseline and at the 6-month follow-up. The blood pressure from baseline to 6 months had significantly decreased (24-h systolic blood pressure from 150.9 ± 16.2 mm Hg to 131.3 ± 21.7 mm Hg, P = 0.008), awakening time systolic blood pressure from 152.1 ± 16.9 mm Hg to 131.7 ± 23.2 mm Hg, P = 0.01, sleep-time systolic blood pressure from 148.1 ± 19.7 mm Hg to 130.0 ± 20.1 mm Hg, P = 0.005). There was a significant reduction in serum noradrenaline levels as well as left ventricular mass index after switching to azilsartan (from 550.1 ± 282.9 pg/mL, to 351.7 ± 152.3 pg/mL, P = 0.002; from 117.0 ± 26.4 g/m(2) to 111.3 ± 23.9 g/m(2), P = 0.01, respectively). Azilsartan had a significantly stronger hypotensive effect than other angiotensin receptor blockers. Thus, the switch to azilsartan might improve prognosis of hemodialysis patients. We suggest that the strong anti-hypertensive effect of azilsartan originated from a combination of primary angiotensin receptor blocker class-effect and a stronger suppression of sympathetic nervous system.

Patient with a massive idiopathic thrombosis in the inferior vena cava.

A 50 year-old man with no significant medical history was admitted for dyspnea and left femoral swelling. Contrast-enhanced computed tomography revealed pulmonary thromboembolism (PTE) and a thrombus in the inferior vena cava (IVC). The thrombus extended from the proximal IVC to the left popliteal vein. Therefore, we decided that an IVC filter insertion was difficult to indicate. Urgent IVC and peripheral vein thrombectomy was performed under cardiopulmonary bypass. On postoperative day 1, venous ultrasonography showed residual deep vein thrombosis in the left external iliac-femoral vein and the popliteal vein. The IVC filter insertion was performed to prevent the recurrence of PTE.

Cough syncope induced by gastroesophageal reflux disease.

A 52-year-old Japanese man was admitted to our hospital for evaluation of syncope and convulsions. An electrocardiogram on admission revealed normal sinus rhythm. However, after repeated bouts of coughing, the heart rate showed bradycardia associated with convulsion. He was diagnosed with cough syncope secondary to laryngopharyngitis, which was caused by gastroesophageal reflux disease (GERD). Once the patient was administrated lansoprazole (Takeda Pharmaceutical Co., Osaka, Japan) for GERD, the syncope disappeared. The causes of syncope are diverse and may manifest in disorders of different organ systems in the body. Therefore, clinicians should perform a careful whole body examination to obtain the correct diagnosis.

Comparison of temporary occlusion and aspiration system versus the conventional method during coronary stenting for acute myocardial infarction.

This study evaluated the effects of the temporary occlusion and aspiration device GuardWire on percutaneous coronary intervention for acute myocardial infarction. This device brought about a significant reduction in the no-reflow phenomenon and improvement in ST resolution compared with conventional percutaneous coronary intervention.

Mechanisms of acute lumen gain following cutting balloon angioplasty in calcified and noncalcified lesions: an intravascular ultrasound study.

Several studies have shown that mechanisms for lumen enlargement following conventional balloon angioplasty (BA) consist of plaque reduction and vessel expansion. To assess the mechanisms of lumen enlargement after Cutting Balloon (CB) angioplasty, intravascular ultrasound images were analyzed in 180 lesions (89 CB and 91 BA). External elastic membrane (EEM) cross-sectional area (CSA), lumen CSA, and plaque plus media (P+M) CSA were measured before and after angioplasty. In the CB group, lower balloon pressure was utilized (P < 0.0001). DeltaP+M CSA was significantly larger (P = 0.02) and deltalumen CSA showed a trend toward being larger (P = 0.07) compared to BA group. For noncalcified lesions, CB resulted in a larger deltaP+M CSA (P < 0.05) and a smaller deltaEEM CSA (P = 0.10) than BA. For calcified lesions, deltalumen CSA was significantly larger in the CB group (P < 0.05) without significant differences in deltaEEM CSA and deltaP+M CSA. Dissections complicated with calcified lesions were associated with larger deltalumen CSA for the CB group. In conclusion, for noncalcified lesions, CB achieves similar luminal dimensions with larger plaque reduction and less vessel expansion compared to BA. On the other hand, for calcified lesions, the CB achieves larger lumen gain, especially in lesions with evidence of dissections.

Impact of deep vessel wall injury and vessel stretching on subsequent arterial remodeling after balloon angioplasty: a serial intravascular ultrasound study.

BACKGROUND: Arterial remodeling has been shown to be responsible for lumen narrowing after nonstent interventions. METHODS: To examine the impact of deep vessel wall injury (DI) after balloon angioplasty on the subsequent vessel remodeling process, we performed serial intravascular ultrasound (IVUS) analysis in 47 native coronary artery lesions that underwent balloon angioplasty. An IVUS study was performed before and after balloon angioplasty and repeated at follow-up. Vessel and lumen area were measured at the narrowest site before intervention. Plaque area was calculated as vessel area minus lumen area. DI was defined as the presence of plaque/vessel wall fracture deep in the medial layer (sonolucent zone by IVUS) after angioplasty. RESULTS: After angioplasty, DI was present in 18 (38%, DI group) and absent in 29 (62%, non-DI group) of lesions. During follow-up, changes in vessel area in the DI group were significantly larger than in the non-DI group (P =.007). There were no significant differences in changes in plaque area. A trend toward greater late lumen loss was observed in the non-DI group (P =.05). In the DI group, changes in lumen area correlated better with changes in vessel area (r = 0.81, P <.0001) than with changes in plaque area (r = 0.32, P =.20). However, in the non-DI group, changes in lumen area correlated with changes in plaque area (r = -0.55, P =.002), but not with changes in vessel area (r = 0.30, P =.11). CONCLUSIONS: Deep vessel wall injury after balloon angioplasty is associated with the magnitude of the subsequent vessel remodeling process. The differences in the remodeling process may have implications regarding adjunctive therapies to prevent restenosis after balloon angioplasty.