Responsiveness to dobutamine stimulation in patients with left ventricular apical ballooning syndrome.

To investigate the underlying mechanisms of the left ventricular (LV) apical ballooning syndrome, we evaluated the functional responsiveness to dobutamine stimulation in patients with the syndrome. Over a 22-month period, 11 consecutive patients with the apical ballooning syndrome were referred to our institution. All 11 patients were women and 57 to 85 years of age (mean 73 +/- 10). Among them, 10 patients underwent low-dose dobutamine echocardiography within 24 hours after admission (17 +/- 8 hours). Echocardiography was repeated in the convalescent phase (48 +/- 33 days) to assess functional outcome. In the resting state, all patients showed akinetic wall motion in the midportion of the left ventricle and apical left ventricle. After low-dose dobutamine infusion, akinetic wall motion detected at rest did not show any improvement despite the hypercontractile basal LV wall. In the convalescent phase, LV dysfunction was not observed on echocardiography in all 11 patients. The LV apical ballooning syndrome has a unique feature that reversible dysfunction lacks functional amelioration during dobutamine administration. In conclusion, this finding suggests that the pathophysiologic mechanisms of the syndrome appear to be distinct from those of myocardial stunning after transient ischemia, and catecholamine-mediated cardiac toxicity may play a role in the development of the syndrome.

[A 95-year-old female with autopsy-proven cerebral necrosis due to candidiasis who developed stroke-like manifestations].

A 95-year-old woman complained of sudden onset of disturbance of consciousness and right hemiparesis on April 20, 2003 and was admitted on the next day. She was drowsy and showed moderate right motor and sensory hemiparesis. The blood laboratory tests showed slight inflammatory reaction. A low density area was found in the left basal ganglia by brain CT, which was also coincided with the high signal region in T2, FLAIR and diffusion-MR images. The MRA of the intracerebral arteries presented no remarkable abnormality. The hemiparesis and impaired consciousness improved partially in the following week. However, she did not fully recover, since aspiration pneumonia and mild generalized inflammation continued. Percutaneous gastrostomy and intravenous hyperalimentation were started to improve her nutrition. The moderate inflammatory state persisted for several weeks. Her blood pressure suddenly fell and she died on June 12. Autopsy showed a mildly brownish and necrotic lesion from the left caudate to the putamen through the internal capsule. There was no liquefaction. On the microscopic examination, the necrosis surrounded by small vessels was consisted of numerous neutrophils and macrophages with pseudohypha and blastospore of candida. Small fragments of fungus were phagocytosed by macrophages. Small abscesses and necrotic foci due to candidiasis were observed in the bladder, kidneys, lungs, myocardium and thyroid gland. In this case, cerebral candidiasis probably occurred via hematogenous dissemination from a primary focus in the urinary tract. The intracerebral arteries revealed rather mild atherosclerotic changes and there was no occlusion by thromboembolism. Intracerebral lesion was diagnosed as candidiasis and there was no cerebral infarction by thromboembolism. If the infection occurred after cerebral infarction, there should not be any inflammatory reaction in the center of necrotic area. There have been few reports of cerebral candidal infection in patients without diabetes mellitus or immunosuppressive conditions. None of them had been diagnosed before death. Caution should be exercised for the presence of systemic candidiasis in elderly patients who are bedridden and with continuous low grade inflammatory reactions.