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BACKGROUND Hypertensive patients are at increased risk of diastolic dysfunction. The hypothesis of this study was that addition of amlodipine would be superior to valsartan in improving diastolic dysfunction associated with hypertension. METHODS In this randomized trial, we randomly assigned 104 controlled, hypertensive patients with diastolic dysfunction to receive either amlodipine 2.5 mg or valsartan 40 mg, in addition to antihypertensive therapy. The primary end point was the change in the ratio of early mitral inflow velocity to early mitral annular relaxation velocity (E/E') from baseline to the 6-month follow-up. Secondary end points included changes in systolic blood pressure (SBP), left ventricular (LV) mass index, and left atrial volume index. RESULTS SBP decreased significantly from baseline in both treatment groups (p < 0.001). E/E' decreased significantly from 13.0 ± 2.2 to 12.0 ± 2.7 in the amlodipine arm and from 14.4 ± 4.3 to 12.7 ± 3.7 in the valsartan arm (p < 0.01 in both groups). The change of E/E' was not significantly different between treatment groups (p = 0.25). There were also no significant between-group differences regarding the changes in SBP, LV mass index, and left atrial volume index. Two patients (3.8%) in the amlodipine group and 1 (16%) in the valsartan group had serious adverse event. CONCLUSIONS In this randomized trial involving controlled hypertensive patients, addition of amlodipine or valsartan was associated with an improvement of diastolic dysfunction, but the effects on diastolic dysfunction did not differ significantly between the treatment groups.

Cardiac metastasis from renal cell carcinoma (RCC) without inferior vena cava (IVC) involvements is extremely rare with few reported cases. Sarcomatoid RCC with rhabdoid feature is a rare pathologic type of RCC having aggressive behavior due to great metastatic potential. Here, we report a case of rapidly growing cardiac metastasis of RCC which brought on right ventricular outflow tract (RVOT) obstruction without IVC and right atrial involvement in a 61-year-old woman. Cardiac arrest occurred during radical nephrectomy and echocardiography revealed mass nearly obstructing the RVOT which was not recognized by preoperative echocardiography 1 month ago. Postoperative immunohistochemical evaluation of renal mass revealed sarcomatoid RCC with rhabdoid feature.

A 31-year-old woman referred to evaluate the cause of sudden dizziness. She had no history of diabetes, hypertension, arrhythmias or stroke. Auscultation showed clear lung sound and no cardiac murmurs. Chest radiography and electrocardiogram did not show any abnormalities. Laboratory tests for hypercoagulability and vasculitis were all negative. In the previous hospital, she took brain magnetic resonance imaging, which revealed newly developed multiple right cerebellar infarction (Fig. 1). Transthoracic echocardiography and transesophageal echocardiography (TEE) for the evaluation of embolic source showed the right-to-left shunt, but the cause of shunt was inconclusive. After transfer, we repeated contrast echocardiography using agitated saline and reaffirmed a delayed appearance of a substantial amount of microbubbles in the left atrium (Fig. 2). However, we could not depict a passage of microbubbles through the gap between interatrial septum to confirm the presence of patent foramen ovale (PFO). Thus, we evaluated all the pulmonary veins, one by one during TEE and finally revealed the microbubbles in a row coming from the left lower pulmonary vein (Fig. 3 and Supplementary movie 1). These findings suggested the presence of a pulmonary arterio-venous fistula (PAVF) in the left lower pulmonary lobe, possibly causing paradoxical embolisms. The diagnosis was confirmed by a computed tomography pulmonary angiography which revealed the fistula located posteriorly in the left lower pulmonary lobe (Fig. 4, arrow). After successful occlusion of the fistula, the patient was discharged with warfarin. Fig. 1 Diffusion-weighted magnetic resonance imaging of brain shows multiple high-intensity signals in the right cerebellum. Fig. 2 Contrast transthoracic echocardiogram illustrating delayed right-to-left passage of agitated saline contrast (microbubbles) in left atrium and left ventricle. Fig. 3 Color flow imaging of transesophageal echocardiogram showing the inflow from left lower pulmonary vein (LLPV) and left upper pulmonary vein (LUPV). Contrast echocardiogram showing microbubbles in a row (arrows) draining into left atrium from LLPV but ... Fig. 4 Chest computed tomography angiogram with volume rendered reconstruction showing the fistula (arrow) located posteriorly in the left lower pulmonary lobe. Both PFO and PAVF could contribute to the development of right-to-left shunt.1) Presence of PAVF and the draining pulmonary vein could be accurately identified by TEE. We need to routinely examine the presence of PAVF during TEE in the evaluation of embolic source.

A 36-year-old male patient with no remarkable medical history was admitted to our hospital for a health check up. On chest radiography, bilateral aortic notches at the level of aortic arch were shown suggesting aortic arch anomaly without any clinical symptoms. Two aortic arches were almost same-in-size on suprasternal view of transthoracic echocardiography. In addition, multidetector computed tomography showed balanced type double aortic arch forming a complete vascular ring which encircled the trachea and esophagus. The trachea was slightly compressed by the vascular ring whereas the esophagus was intact. Nevertheless, the pulmonary function test was normal. The patient was discharged from hospital with instructions for periodic follow-up.

Intramyocardial hematoma is known to be associated with myocardial infarction, chest trauma, coronary artery bypass operation, and complication of percutaneous coronary intervention (PCI). We describe here a rare case of 50-year-old man with a huge right ventricular (RV) wall hematoma which was newly developed two hours after PCI. The patient was treated conservatively with a successful outcome. We discuss plausible mechanisms for the development of RV wall hematoma and treatment options for the case.