Beta-blocker stress echocardiography in an aortic stenosis patient with associated left ventricular outflow tract obstruction.

An 80-year-old man visited our hospital because of dyspnea on exertion from 6 months ago. Echo Doppler study showed severe calcification in the aortic valve with restricted movement and the sigmoid septum causing obstruction at the LV outflow tract (LVOT). Considering the aortic valve area (AVA) might have been inaccurately estimated, we carried out beta-blocker stress echocardiography. The transaortic pressure gradient and AVA were respectively calculated as 52 mmHg and 0.90 cm(2) before propranolol administration and as 64 mmHg and 0.86 cm(2) after propranolol administration. Thus, beta-blocker stress echocardiography may provide an accurate assessment of AS if the LVOT obstruction is concomitant.

Multiple complex coronary atherosclerosis in diabetic patients with acute myocardial infarction: a three-vessel optical coherence tomography study.

AIMS: The main cause of acute myocardial infarction (AMI) is the disruption of a thin-cap fibroatheroma (TCFA) and subsequent thrombosis. Mortality increases in diabetic patients due to cardiovascular events; there may be differences in the vulnerable plaques between diabetic and non-diabetic patients. We used optical coherence tomography (OCT) to assess the incidence of vulnerable plaques in diabetic patients with AMI. METHODS AND RESULTS: OCT was performed in all three major coronary arteries of 70 AMI patients: 48 non-diabetic and 22 diabetic patients. The OCT criterion for TCFA was the presence of both a lipid-rich plaque composition and a fibrotic cap thickness of <65 µm. A ruptured plaque contains a cavity in contact with a lumen and a residual fibrous cap. OCT identified 68 plaque ruptures (1.0 per patient; range, 0-3) and 162 TCFAs (2.3 per patient; range, 0-5). The incidences of plaque rupture and TCFA at culprit lesions were similar. However, non-culprit-lesion TCFAs were observed more frequently in diabetic patients than in non-diabetic patients. CONCLUSIONS: Although the prevalence of vulnerable plaque in culprit lesions was similar between diabetic and non-diabetic patients, vulnerable plaques were observed in non-culprit lesions more in diabetic patients than in non-diabetic patients.

The impact of plaque characterization assessed by intravascular ultrasound on myocardial perfusion after primary angioplasty in patients With ST-segment elevation myocardial infarction.

BACKGROUND: Previous studies described that inadequate tissue perfusion after primary angioplasty in ST-elevation myocardial infarction (STEMI) patients is associated with adverse cardiac events. This study evaluated whether plaque morphological intravascular ultrasound (IVUS) characteristics affects tissue perfusion after stent implantation in STEMI patients. METHODS AND RESULTS: A total of consecutive 306 STEMI patients who underwent primary angioplasty with IVUS were analyzed. Maximum ST-segment elevation before angioplasty was compared with ST-segment levels 60min after angioplasty. Percent ST-segment resolution (STR) was calculated and categorized as complete (>70%), partial (30-70%), and absent (<30%). Qualitative and quantitative IVUS analyses were performed using standard methods. Plaque with ultrasound attenuation was defined as IVUS finding with backward signal attenuation behind plaque >180° without dense calcium. One-hundred-fifty patients had complete, 101 had partial, and 55 had absent STR. The incidence of in-hospital death tended to be higher in absent STR than in partial and complete STR groups. Multivariate analysis indicated that remodeling index (P=0.004), the presence of ultrasound attenuation (P=0.02), percentage stent expansion (P=0.03), and the presence of deep calcium (P=0.049) were the independent predictors related to the occurrence of absent STR after angioplasty. CONCLUSIONS: Positive vessel remodeling, plaque with ultrasound attenuation >180°, deep calcium, and stent overexpansion as assessed by IVUS are associated with the absence of STR after primary angioplasty in patients with STEMI.

Loop diuretic precipitated beriberi in a patient after pancreaticoduodenectomy: a case report.

Upper gastrointestinal tract surgery and diuretic use are 2 unrecognized causes of thiamine (vitamin B1) deficiency. Upper gastrointestinal tract surgery decreases the thiamine absorption, and diuretic use increases urinary excretion of thiamine. We present a case of a patient with a history of pancreaticoduodenectomy who had development of beriberi by diuretic use. A 68-year-old man was referred to our hospital because of pretibial pitting edema, foot numbness, and gait disturbance. He had a history of pancreaticoduodenectomy 8 years before and had been taking loop diuretics for 2 months. He had signs of polyneuropathy and hyperkinetic heart. Beriberi was suspected, and thiamine supplementation was started immediately. Edema disappeared within several days, and signs of polyneuropathy gradually subsided. Because diuretics enhance urinary thiamine excretion, practitioners should use caution for thiamine deficiency when they prescribe diuretics for patients who have a history of upper gastrointestinal surgery and potentially have latent thiamine deficiency.

Characterization of left ventricular filling abnormalities and its relation to elevated plasma brain natriuretic peptide level in acute to chronic diastolic heart failure.

BACKGROUND: Although Doppler left ventricular (LV) filling abnormalities have been extensively analyzed in patients with systolic heart failure (SHF), they have not yet been well characterized in patients with acute to chronic diastolic heart failure (DHF) in the light of plasma brain natriuretic peptide (BNP) levels. METHODS AND RESULTS: In 25 patients presenting with acute DHF and 25 with acute SHF, echo Doppler parameters and plasma BNP levels were obtained on admission and in the chronic stage. The mitral E/A ratio was lower in DHF patients than in SHF patients in the acute stage (1.3 +/-0.4 vs 1.8+/-0.9, p<0.05), and in the chronic stage of DHF the ratio decreased with plasma BNP level, but plasma BNP level was still greater than 100 pg/ml in 15 patients (60%). Among patients with DHF the plasma BNP level did not correlate with the mitral E/A ratio or deceleration time (r=0,25, p=NS; r=0,23, p=NS), but did with estimated pulmonary artery systolic pressure (r=0.64, p<0.01). CONCLUSIONS: A restrictive mitral flow velocity pattern is observed in only 25% of patients with DHF, so it is particularly important to recognize pseudonormalization in those with possible DHF. Persistently elevated plasma BNP level is not primarily caused by LV diastolic dysfunction, but by secondary alteration for hemodynamic adjustment (elevated LV end-diastolic pressure) in patients with DHF.