Symmetric peripheral gangrene as an emerging manifestation of polyarteritis nodosa.
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Angiography↗
Biomedical subjects
Yoshihiro Himura
Publications and source records attributed to Yoshihiro Himura.
Late regression of left internal thoracic artery graft stenosis at the anastomotic site without intervention therapy.
OBJECTIVE: Intervention therapy has been recently performed on the left internal thoracic artery graft stenosis. The purpose of this study was to evaluate the natural course of the left internal thoracic artery graft stenosis at the anastomotic site and clarify whether intervention therapy should be performed early after surgery. METHODS: We investigated early angiographic results of the left internal thoracic artery graft in 343 consecutive patients who underwent coronary bypass surgery. In 100 of 343 patients who underwent follow-up angiography, the graft diameter and percentage diameter stenosis at the anastomotic site were compared between early postoperative and follow-up angiography. None of these patients underwent intervention therapy on the left internal thoracic artery graft. RESULTS: Of 343 patients, 46 showed 50% or greater diameter stenosis, and 20 showed 70% or greater diameter stenosis at the anastomotic site. In the 100 patients with follow-up angiography, the graft diameter significantly increased (1.8 +/- 0.4 vs 2.1 +/- 0.5 mm, P < .0001) at follow-up angiography. The percentage diameter stenosis significantly decreased (69% +/- 13% vs 35% +/- 20%, P < .0001) at follow-up angiography in the patients with 50% or greater diameter stenosis at early postoperative angiography. Regression of left internal thoracic artery graft stenosis was detected in most patients with 70% or greater diameter stenosis. CONCLUSIONS: Our study demonstrated that left internal thoracic artery graft stenosis at the anastomotic site at early postoperative angiography might improve without intervention therapy. We should consider the natural course of the left internal thoracic artery graft stenosis in determining the indication of intervention therapy early after surgery.
Adult↗
Cholesterol embolism after cardiac catheterization mimicking infective endocarditis.
We present a 65-year-old man with rheumatic combined valvular heart disease showing persistent fever 3 weeks after diagnostic cardiac catheterization. Infective endocarditis was strongly suspected from the clinical course, however, serial blood cultures were negative. Transesophageal echocardiography, done to investigate vegetation, revealed multiple mobile plaques in the descending aorta. Administration of both steroid and simvastatin improved both symptoms and renal function. Cholesterol embolism should be considered to be one of the possible causes of low-grade fever after cardiac catheterization especially in patients with anticoagulation.
Aged↗
Infective endocarditis developing as uremia.
A 49-year-old man presented with fever and uremic symptoms such as general malaise, leg edema and decreased urine output. He was diagnosed as having infective endocarditis (IE) accompanied by renal failure. Although he had been receiving hemodialysis for a long time, renal function dramatically improved after heart valve replacement. This case suggests that uremia can develop as an initial manifestation of IE and removal of an infected heart valve can improve renal function despite persistent renal failure. From the perspective of recovery of renal function, early surgery should be considered in patients with renal failure following IE.
Anuria↗
Usefulness of high-frequency transthoracic Doppler echocardiography in noninvasive diagnosis of the left internal thoracic artery graft stenosis at the anastomosis.
BACKGROUND: Stenosis of the left internal thoracic artery (LITA) graft, which usually occurs at the site of the anastomosis, can be noninvasively evaluated by the flow pattern in the proximal graft, but the flow pattern is influenced by several other factors. METHODS AND RESULTS: In the present study, LITA graft flow was investigated by high-frequency transthoracic Doppler echocardiography in 75 consecutive patients who underwent postoperative angiography of the LITA graft. The flow velocity was measured at both the anastomosis and proximal to it, and compared with the quantitative angiographic results. Flow at both sites was detected in 61 (81%) of the 75 patients. The diastolic velocity ratio of the anastomosis to the proximal site correlated with the percent diameter stenosis at the anastomosis. A diastolic velocity ratio >2.0 had a high sensitivity, specificity, positive predictive value and negative predictive value for the presence of significant stenosis at the anastomosis of a LITA graft. CONCLUSIONS: High-frequency transthoracic Doppler echocardiography can be used for the noninvasive diagnosis of LITA graft stenosis.
Aged↗
[Efficacy of transesophageal echocardiography in patients with cardiac arrest or shock].
OBJECTIVES: Only a few examinations are available to critically ill patients. We assessed the efficacy of transesophageal echocardiography (TEE) in the management of patients with cardiac arrest or shock. METHODS: Among a total of 2,021 patients who underwent TEE over the past 13 years at our institution, we reviewed 18 patients who underwent TEE during cardiac arrest or shock. RESULTS: TEE was performed in four patients with cardiac arrest and in 14 patients with shock. In 12 (67%) of 18 patients, TEE identified the following abnormalities: aortic dissection in four, ruptured thoracic aortic aneurysm in two, papillary muscle rupture in two, left ventricular free wall rupture in two, postoperative cardiac tamponade in one and ruptured chordae tendineae in one. TEE excluded suspected cardiac abnormality in two other patients. Transthoracic echocardiography could not be performed in 8 of 18 patients, and showed poor quality of images in the remaining 10 patients. Of the 12 patients with a diagnosis based on TEE, three patients died during cardiopulmonary resuscitation, whereas nine patients were treated with emergent surgery and six of these survived to hospital discharge. CONCLUSIONS: TEE is feasible even in patients with cardiac arrest or shock, and can play an important role in establishing the diagnosis and determining the treatment of such patients.
Aged↗
Desipramine attenuates loss of cardiac sympathetic neurotransmitters produced by congestive heart failure and NE infusion.
We reported recently that inhibition of neuronal reuptake of norepinephrine (NE) by desipramine prevented the reduction of sympathetic neurotransmitters in the failing right ventricle of right heart failure animals. In this study, we studied whether desipramine also reduced the sympathetic neurotransmitter loss in animals with left heart failure induced by rapid ventricular pacing (225 beats/min) or after chronic NE infusion (0.5 microg. kg(-1). min(-1)). Desipramine was given to the animals for 8 wk beginning with rapid ventricular pacing or NE infusion. Animals receiving no desipramine were studied as controls. We measured myocardial NE content, NE uptake activity, and sympathetic NE, tyrosine hydroxylase, and neuropeptide Y profiles by histofluorescence and immunocytochemical techniques. Effects of desipramine on NE uptake inhibition were evidenced by potentiation of the pressor response to exogenous NE and reduction of myocardial NE uptake activity. Desipramine treatment had no effect in sham or saline control animals but attenuated the reduction of sympathetic neurotransmitter profiles in the left ventricles of animals with rapid cardiac pacing and NE infusion. In contrast, the panneuronal marker protein gene product 9.5 profile was not affected by either rapid pacing or NE infusion, nor was it changed by desipramine treatment in the heart failure animals. The study confirms that excess NE contributes to the reduction of cardiac sympathetic neurotransmitters in heart failure. In addition, it shows that the anatomic integrity of the sympathetic nerves is relatively intact and that the neuronal damaging effect of NE involves the uptake of NE or its metabolites into the sympathetic nerves.
Adrenergic Fibers↗
Differential pre- and postsynaptic effects of desipramine on cardiac sympathetic nerve terminals in RHF.
Right heart failure (RHF) is characterized by chamber-specific reductions of myocardial norepinephrine (NE) reuptake, beta-receptor density, and profiles of cardiac sympathetic nerve ending neurotransmitters. To study the functional linkage between NE uptake and the pre- and postsynaptic changes, we administered desipramine (225 mg/day), a NE uptake inhibitor, to dogs with RHF produced by tricuspid avulsion and progressive pulmonary constriction or sham-operated dogs for 6 wk. Animals receiving no desipramine were studied as controls. We measured myocardial NE uptake activity using [(3)H]NE, beta-receptor density by [(125)I]iodocyanopindolol, inotropic responses to dobutamine, and noradrenergic terminal neurotransmitter profiles by glyoxylic acid-induced histofluorescence for catecholamines, and immunocytochemical staining for tyrosine hydroxylase and neuropeptide Y. Desipramine decreased myocardial NE uptake activity and had no effect on the resting hemodynamics in both RHF and sham animals but decreased myocardial beta-adrenoceptor density and beta-adrenergic inotropic responses in both ventricles of the RHF animals. However, desipramine treatment prevented the reduction of sympathetic neurotransmitter profiles in the failing heart. Our results indicate that NE uptake inhibition facilitates the reduction of myocardial beta-adrenoceptor density and beta-adrenergic subsensitivity in RHF, probably by increasing interstitial NE concentrations, but protects the cardiac noradrenergic nerve endings from damage, probably via blockade of NE-derived neurotoxic metabolites into the nerve endings.
Adrenergic Uptake Inhibitors↗