Doctor of Medicine, Osaka University (2008)
Peter Fitzgerald, Postdoctoral Faculty Sponsor
Increased level of serum catecholamines in the acute phase was reported to be a feature of takotsubo cardiomyopathy (TC). We report a TC case with pheochromocytoma, which caused a stir in the diagnosis of TC and suggests the importance of screening for a catecholamine-producing tumor. A female patient was referred to our emergency department due to ongoing chest pain. Coronary angiography showed no abnormality; however, subsequent left ventriculography showed basal hyperkinesis and apical ballooning, which completely recovered in 2 weeks. She experienced significant emotional stress on the eve of her admission, to which the diagnosis of TC was attributed. Although serum catecholamine levels on admission in our case were higher than on day 14, the value on day 14 was much higher than the normal range in our patient. The screening abdominal computed tomography scan revealed a left adrenal mass, which was diagnosed as pheochromocytoma by 24-hour urinary excretion of catecholamine and (131)I-MIBG scintigraphy. The mass was successfully resected and pathological findings supported the diagnosis. In our case, emotional stress was thought to be the direct trigger to develop TC by exceeding the threshold of catecholamine-induced cardiomyopathy. Screening for a catecholamine-producing tumor through careful history-taking and measuring catecholamines at a follow-up stage were important clinical aspects in this case and may well be for others.
View details for PubMedID 24907091
Nicorandil, an ATP sensitive potassium channel opener, may reduce the incidence of microvascular dysfunction after percutaneous coronary intervention (PCI) by dilating coronary resistance vessels. The aim of the study was evaluation of the impact of the administration of intravenous nicorandil on measuring the index of microcirculatory resistance (IMR) in PCI to patients with stable angina pectoris (SAP).Intravascular ultrasound (IVUS), fractional flow reserve (FFR), IMR and blood examination (CK-MB), cardiac troponin I (cTnI) immediately post-PCI (and 24 hours later) were performed in 62 consecutive patients with SAP undergoing PCI. FFR and IMR were measured simultaneously with a single coronary pressure wire. IMR was defined as Pd/coronary flow (or Pd* mean transit time) at peak hyperaemia. Patients were randomised to the control (n=29), or nicorandil group (n=33). In the nicorandil group, nicorandil was intravenously administered as a 6 mg bolus injection just before PCI and as a constant infusion at 6 mg/hour for 24 hours thereafter. All volumetric IVUS parameters and FFR were similar between the two groups both pre- and post-PCI. However, IMR immediately post-PCI and cTnI 24 hours post-PCI were significantly higher in the control group compared to the nicorandil group (IMR: 25.4±12.1 vs. 17.9±9.1 units, and cTnI: 0.21±0.13 vs. 0.12±0.08 ng/mL, for control vs. nicorandil). The incidence for cTnI elevation more than fivefold the normal range (>0.20 ng/mL) was significantly larger in the control group than in the nicorandil group (41% vs. 12%, p<0.01). Additionally, the control group showed a closer correlation between plaque volume reduction during stenting as assessed by volumetric IVUS, and cTnI elevation than the nicorandil group (r=0.55 vs. 0.42, p<0.001 for control vs. nicorandil).In patients undergoing successful coronary stenting for stable angina, administration of nicorandil is associated with reduced microvascular dysfunction induced by PCI.
View details for DOI 10.4244/EIJV9I9A178
View details for PubMedID 24457276
View details for DOI 10.2217/ica.13.88
A case of acute myocardial infarction (AMI) due to thrombus in the left coronary cusp to the ascending aorta is described. There was no clinical evidence of coagulopathy, immunodisability, or local erosive lesion of the aortic and sinus of Valsalva wall macroscopically. Secondary polycythemia, induced by heavy smoking, was the likely cause of the myocardial infarction. Although this may be a rare case, intraaortic thrombus should be considered in the differential diagnosis of the causes of AMI.
View details for Web of Science ID 000324872700018
View details for PubMedID 23913610
The previous OLIVUS trial reported a positive role in achieving a lower rate of coronary atheroma progression through the administration of olmesartan, an angiotension-II receptor blocking agent (ARB), for stable angina pectoris (SAP) patients requiring percutaneous coronary intervention (PCI). However, the benefits between ARB administration on long-term clinical outcomes and serial atheroma changes by IVUS remain unclear. Thus, we examined the 4-year clinical outcomes from OLIVUS according to treatment strategy with olmesartan.Serial volumetric IVUS examinations (baseline and 14 months) were performed in 247 patients with hypertension and SAP. When these patients underwent PCI for culprit lesions, IVUS was performed in their non-culprit vessels. Patients were randomly assigned to receive 20-40mg of olmesartan or control, and treated with a combination of β-blockers, calcium channel blockers, glycemic control agents and/or statins per physician's guidance. Four-year clinical outcomes and annual progression rate of atherosclerosis, assessed by serial IVUS, were compared with major adverse cardio- and cerebrovascular events (MACCE).Cumulative event-free survival was significantly higher in the olmesartan group than in the control group (p=0.04; log-rank test). By adjusting for validated prognosticators, olmesartan administration was identified as a good predictor of MACCE (p=0.041). On the other hand, patients with adverse events (n=31) had larger annual atheroma progression than the rest of the population (23.8% vs. 2.1%, p<0.001).Olmesartan therapy appears to confer improved long-term clinical outcomes. Atheroma volume changes, assessed by IVUS, seem to be a reliable surrogate for future major adverse cardio- and cerebrovascular events in this study cohort.
View details for DOI 10.1016/j.atherosclerosis.2011.10.013
View details for Web of Science ID 000298374800022
View details for PubMedID 22119063