Search

Objective: The degree of myocardial technetium--pyrophosphate (Tc-PYP) accumulation in cardiac amyloidosis is conventionally evaluated by the PYP score. This method involves qualitative visual evaluation on two-dimensional images. Here, we performed three-dimensional quantitative analysis using software developed in our laboratory. Methods: We performed dual myocardial imaging using thallium--chloride (Tl-Cl) and Tc-PYP in cases of suspected cardiac amyloidosis and calculated the PYP accumulation rates of all myocardial pixels showing Tc-PYP accumulation. We defined this procedure as quantitative evaluation of the degree of Tc-PYP accumulation in the myocardium. Patients were divided into two groups with and without a diagnosis of cardiac amyloidosis, and we examined the PYP accumulation rates in both groups. In addition, we examined the PYP scores of the two groups by conventional qualitative evaluation. Results: The PYP scores of the cardiac amyloidosis group were significantly higher than those of the other group. The PYP accumulation rates of the cardiac amyloidosis group were significantly higher than those of the other group. There were significant differences in the PYP accumulation rate and PYP score between the two groups. There was considered to be a threshold between the two groups in the case of the PYP accumulation rate. Conclusions: When the threshold of the PYP score was defined as 3+ and that of the PYP accumulation rate as 41.5 %, the sensitivity of the PYP score and PYP accumulation rate was 84.6 %. However, the specificity of the PYP accumulation rate was higher than that of the PYP score. Quantitative evaluation by the PYP accumulation rate of the degree of Tc-PYP accumulation in the myocardium may be useful in the diagnosis of cardiac amyloidosis. [ABSTRACT FROM AUTHOR]

Background: Left atrial (LA) enlargement has been documented to occur in hypertension (HT), and has been an index for evaluating the diastolic function of the left ventricle. Enlargement of the LA is one of the vital factors that induce heart failure and atrial fibrillation (AF) in patients with HT. Methods and subjects: 130 treated hypertensive patients were enrolled. All recruits participated in an echocardiogram, electrocardiogram, a routine blood examination including brain natriuretic peptide (BNP), and physical examinations. Results: Left ventricular mass (LVM) indexed to height2.7 had a significant positive correlation with left atrial volume index (LAVI) (p < 0.0001 ), as well as natural logarithm BNP (p < 0.001 ). Blood pressure levels were not associated with LAVI, neither body mass index nor age. LAVI had a positive correlation with factors involving the left ventricle volume, LVM, and right ventricle systolic pressure (RVSP) (r = 0.687, p < 0.0001 ). The parameters of LV diastolic function were positively but weakly associated with LA size. In the subgroup of LAVI, the evidence of paroxysmal atrial fibrillation (PAF): LAVI <32 ml/m² had no PAF, whereas the incidence of PAF was 7.5%, 11.4%, and 15.2%, respectively in the LAVI > 32 ml/m² group. Of anti-hypertension drugs, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers had a tendency to reduce LAVI; however, there was no statistical significance within the groups. Conclusions: Left ventricular volume and mass are independent factors affecting LAVI in treated HT. The incidence of PAF is associated with LA size. In patients with treated HT, LA size may be a useful surrogate marker for monitoring the effectiveness of medical therapy and occurrence of AF. [ABSTRACT FROM AUTHOR]

Traumatic asphyxia is a crush injury of the chest characterized by facial edema, cyanosis, conjunctival hemorrhage, and petechiae on the face and chest. The prognosis depends on the duration of chest compression and early cardiopulmonary resuscitation after cardiopulmonary arrest. Here we report a case of full recovery from cardiopulmonary arrest caused by traumatic asphyxia. The chest of a 56-year-old man was compressed by a machine while working. Immediately, his colleague started cardiopulmonary resuscitation, which was successful. When he was admitted to our hospital, his consciousness level was E1V2M2(Glasgow coma scale). Our treatment included therapeutic hypothermia, the duration of which was 24 hours at 34 °C. Rewarming his body to 36 °C took place over 48 hours. Thereafter, he recovered completely and was discharged on the 12th hospital day without neurologic sequela. Therapeutic hypothermia was possibly effective in this case.