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Y Koiwaya

Publications and source records attributed to Y Koiwaya.

At least 19 recordsLinked to original sources

Secretion of proadrenomedullin N-terminal 20 peptide from cultured neonatal rat cardiac cells.

Proadrenomedullin N-terminal 20 peptide (PAMP) is generated from post-transcriptional enzymatic processing of a 185-amino acid precursor for adrenomedullin (AM), a potent vasodilator peptide. We have reported that AM is secreted from cultured neonatal rat cardiac myocytes and fibroblasts, and that secreted AM modulates the growth of these cells; however, it is unknown whether or not the cardiac cells produce PAMP. In this study, we examined the production of PAMP in cultured neonatal rat cardiac myocytes and fibroblasts. Both the cardiac myocytes and fibroblasts cultured with serum-free media secreted PAMP time-dependently at rates of 5.7+/-0.9 fmol/10(5) cells/40 h and 8.4+/-0.7 fmol/5x10(4) cells/48 h (mean+/-SD), respectively. Reverse-phase high performance liquid chromatography showed that immunoreactive PAMP secreted from these cells was identical to PAMP[1-20], a whole active molecule. PAMP and AM secretions were significantly (P<0.01) stimulated by 10(-6) mol/L angiotensin II (Ang II) and 10% fetal bovine serum (FBS) in myocytes and fibroblasts, whereas the ratio of PAMP to AM secretion in the myocytes was smaller than that of the fibroblasts. These results suggest that PAMP is secreted along with AM from rat cardiac myocytes and fibroblasts, and the secretion is augmented by the growth-promoting stimuli of Ang II and FBS for these cells.

Adrenomedullin↗

Roles of protein kinase C and Ca2+-dependent signaling in angiotensin II-induced adrenomedullin production in rat cardiac myocytes.

OBJECTIVES: We showed that angiotensin II stimulates adrenomedullin production in cultured neonatal rat cardiac myocytes, and that the secreted adrenomedullin inhibits hypertrophy of the myocytes, although the intracellular mechanisms of adrenomedullin production are still unknown. Since protein kinase C (PKC) and the Ca2+ signaling system are involved in cardiac hypertrophy, we examined the roles of these intracellular signaling systems in the production of adrenomedullin by myocytes. METHODS: Cultured neonatal rat cardiac myocytes were incubated with agonists or antagonists of PKC and Ca2+ signaling systems for 24 h. Adrenomedullin secreted into the medium and adrenomedullin mRNA expression were measured by radioimmunoassay and quantitative polymerase chain reaction, respectively. RESULTS: Both phorbol-12-myristate-13-acetate (PMA), a PKC activator and A23187, a calcium ionophore, significantly increased adrenomedullin mRNA expression and secretion from the myocytes. The induction of adrenomedullin secretion by PMA was abolished by H7, a PKC inhibitor, and by downregulation of PKC induced by pre-incubation with PMA. Similarly, the stimulation of adrenomedullin secretion by 10(-6) mol/l angiotensin II was significantly reduced following the inhibition or downregulation of PKC activity in the myocytes. Blockade of the L-type Ca2+ channel and chelation of intracellular Ca2+ both resulted in a significant reduction of the stimulation of adrenomedullin secretion by angiotensin II. In addition, the secretion was significantly attenuated by inhibitors of calmodulin (W-7) and calmodulin kinase II (KN-62), and slightly attenuated by FK506, a calcineurin inhibitor. CONCLUSIONS: These results suggest that PKC and the Ca2+/calmodulin signaling systems are involved in angiotensin II-induced adrenomedullin secretion from rat cardiac myocytes.

Adrenomedullin↗

Microvascular angina in a patient with aortic stenosis.

A 39-year-old woman had exercise-induced ST segment depression associated with chest pain. Cardiac evaluation revealed moderate aortic stenosis (AS), related to the bicuspid valves, with an aortic mean pressure gradient of 22 mmHg, a calculated aortic valve area of 1.3 cm2 and normal left ventricular (LV) peak systolic and end-diastolic pressures, but no LV hypertrophy, resulting in normal LV wall stress. Although the coronary arteries were angiographically normal, rapid atrial pacing and an intracoronary papaverine injection revealed a significantly decreased coronary flow reserve (CFR), which may have played an important role in the pathogenesis of angina pectoris in this patient. Though the CFR is usually decreased in patients with AS, as well as in microvascular angina, in this particular case, it appeared to have decreased as a consequence of microvascular dysfunction rather than of AS-related mechanisms.

Adult↗

[A new protocol of dual energy acquisition on stress 201Tl and rest 99mTc-tetrofosmin myocardial scintigraphy].

We carried out stress 201Tl (Tl) and rest 99mTc-tetrofosmin (TF) myocardial scintigraphy with dual energy acquisition in 24 patients with suspected ischemic heart disease performed coronary arteriography and elucidated the sensitivity of this method. One hour after light meal eating, TF (555 MBq) was injected intravenously at rest and after 3 minutes from injection of TF exercise or pharmacologic stress was performed. During stress Tl (111 MBq) was injected intravenously before end-point or at adequate point of pharmacologic stress. Dual energy acquisition using triple energy windows (TEW) was started after 5 minutes (early) and 4 hours (delayed) from stress. The sensitivity (Sn), specificity (Sp) and accuracy (Ac) in diagnosis of non-infarcted branches by using Tl (early)-TF (rest) and Tl (early)-Tl (delayed) were 79% vs. 53% (Sn), 78% vs. 96% (Sp) and 79% vs. 71% (Ac) respectively. Accordance of uptake score of infarcted region between TF (rest) and Tl (delayed) was 70%. In conclusion, this protocol is seemed to be useful as usual protocol for detection of myocardial ischemia and viability during about only 1 hour.

Aged↗

Clinical manifestations of influenza a myocarditis during the influenza epidemic of winter 1998-1999.

OBJECTIVES: The clinical features of myocarditis that developed during the influenza epidemic of winter 1998-1999 were investigated to emphasize the need for medical attention to this disease. METHODS: Nine patients were treated under diagnoses of acute myocarditis during the winter of 1998-1999. Five (two males and three females, mean age 52 +/- 18 years) were examined with myocarditis associated with influenza A. The diagnosis of influenza A myocarditis was based on electrocardiographic and echocardiographic abnormalities, increased creatine kinase levels and at least a four-fold increase in influenza A virus titers using paired sera. RESULTS: All patients had preceding flu-like symptoms and fever. Cardiac involvement developed between 4 and 7 days after the onset of influenza symptoms. Dyspnea progressively worsened in three patients, one went into shock and one had persistent fever, cough and mild dyspnea without apparent cardiac symptoms. Three patients had ST elevation associated with Q waves and one had complete left bundle branch block. The creatine kinase levels were abnormally increased and global wall motion of the left ventricle on echocardiography was decreased in all patients. Two patients had diagnoses of fulminant myocarditis. One patient died of pneumonia following cerebral infarction, but the left ventricular dysfunction normalized in the remaining four patients. CONCLUSIONS: Cardiac involvement occurred between 4 and 7 days after the onset of influenza symptoms, and worsening dyspnea was the most common symptom. Electrocardiography, echocardiography and creatine kinase levels should be checked to determine the potential for cardiac involvement when patients present with suspected influenza associated with worsening dyspnea or prolonged weakness. Increasing the awareness of influenza myocarditis may help in the earlier identification and treatment of this disease during influenza epidemics.

Adult↗

Angiographic features at ischemia- or infarct-related sites in patients with acute coronary syndrome: morphology changing in a relatively short time.

OBJECTIVES: Coronary cineangiography was reviewed in patients with acute coronary syndrome to investigate whether angiographic features at identifiable ischemia- or infarct-related lesions can change in terms of luminal diameter and morphology in a short period after development, and whether the amount of thrombus with/without underlying ruptured plaque is the major determinant. METHODS: The present study included 72 patients with unstable angina, 118 with acute myocardial infarction (< 1 month after onset) and 137 with old myocardial infarction (> or = 1 month after onset). The coronary angiographic findings were compared with those from patients with stable effort angina. The groups of patients were subdivided into two groups based on whether antiplatelet and/or anticoagulant therapy, or fibrinolytic therapy with subsequent anticoagulant agents (antiplatelet and/or anticoagulant, or fibrinolytic therapy) were administered. The morphologies of the ischemia- or infarct-related lesions were classified as totally occlusive, simple (Type I lesion) or complex. Complex lesions were further subdivided into Type IIa lesions indicative of the presence of thrombus accumulation with/without an underlying ruptured atheromatous plaque, e.g., narrowing with irregular, poorly defined or hazy borders, sharp leading or trailing edges that overhang or are perpendicular to vessel walls, and globular endoluminal negative images, Type IIb lesions with two or more serial, closely spaced narrowings together with multiple irregularities, and Type IIc lesions indicative of the presence of some parts of ruptured plaque with a smaller amount of thrombus, e.g., luminal narrowing with extraluminal contrast pooling, single or paired short thin linear radiolucencies with/without a variable degree of outpouching, and narrowing with definite outpouching with/without radiolucency, and Type IId lesions showing narrowing with morphology not included in Type IIa-IIc lesions. The coronary angiographic findings were related to the elapsed time before the coronary angiographic study, and whether each patient underwent antiplatelet and/or anticoagulant, or fibrinolytic therapy. RESULTS: Ischemia- or infarct-related lesions were totally occlusive in 9.7% of patients with unstable angina, 40.7% of those with acute myocardial infarction and 21.9% of those with old myocardial infarction. Total occlusion was significantly more prevalent in patients with acute myocardial infarction than in those with stable effort angina (23.9%, p < 0.05), and total occlusion was more frequent in patients without antiplatelet and/or anticoagulant, or fibrinolytic drugs (50.6% vs 17.1%, p < 0.01). The presence of total occlusion decreased with time after development, and the decrease was more significant with the use of antiplatelet and/or anticoagulant, or fibrinolytic drugs. Type IIa morphology was significantly prevalent immediately after the initial episode, and Type IIa and IIc morphologies increased in the late period, and were more frequent with the use of antiplatelet and/or anticoagulant, or fibrinolytic drugs. CONCLUSIONS: The severity of the luminal diameter at ischemia- or infarct-related lesions sites can progress or even regress in a relatively short period in patients with acute coronary syndrome, and the amount of accumulated thrombus with/without underlying ruptured plaque is a major determinant of luminal diameter narrowing and angiographic morphology.

Adult↗

Differential responses of circulating and tissue adrenomedullin and gene expression to volume overload.

BACKGROUND: Adrenomedullin (AM), which is produced by various tissues and organs, also circulates in the blood. Circulating AM levels increase during disease states such as essential hypertension, heart failure, and renal failure. However, little is known about how circulating AM or AM production responds to volume overload (VOL). METHODS AND RESULTS: Progressive VOL was induced in rats by an aortocaval shunt (AC) or by an aortocaval shunt with banding of the abdominal aorta distal to the shunt (AC + B), which created a larger shunt volume. Plasma and tissue AM concentrations, as well as AM gene expression levels, were measured at 1, 5, and 14 days after operation. Plasma concentrations of atrial natriuretic peptide (ANP), aldosterone, and renin activity (PRA) were also examined. Pulmonary congestion, pleural effusion, and ascites rapidly progressed in the AC + B group, suggesting that VOL caused more rapid heart failure under these conditions. Plasma AM concentrations in the AC + B and AC groups at day 1 compared with those in sham-operated rats were increased by 300% and 140%, respectively, and then gradually declined. The time course of plasma AM over 14 days was similar to that of plasma aldosterone and PRA, but not of plasma ANP or intracardiac filling pressure. The increase in plasma AM was accompanied by upregulated AM gene expression in the lung and aorta and by decreased AM concentrations in the atrium, ventricle, and adrenal gland. Cardiac AM gene expression levels were increased in the hypertrophied ventricles of AC and AC + B rats. CONCLUSIONS: The major findings of the present study were 1) a rapid increase in plasma AM after the imposition of VOL in association with increased plasma aldosterone and PRA, 2) the contribution of several organs to this increase, and 3) a late increase in the AM messenger RNA (mRNA) level in the ventricles as VOL-induced ventricular hypertrophy developed.

Adrenomedullin↗

Diastolic wall stress and ANG II in cardiac hypertrophy and gene expression induced by volume overload.

We investigated the effects of diastolic wall stress (WS) and angiotensin II (ANG II) on the left ventricular (LV) hypertrophy (LVH) induced by volume overload and on the gene expression of LV adrenomedullin (AM) and atrial natriuretic peptide (ANP) in volume overload. Diastolic WS was pharmacologically manipulated with (candesartan) or without (calcium channel blocker manidipine) inhibition of ANG II type 1 receptors in aortocaval-shunted rats over 6 wk. Diastolic WS reached a plateau at 2 wk and subsequently declined regardless of further LVH. Although diastolic WS was decreased to a similar extent by both compounds, candesartan blunted LVH over 6 wk, whereas manidipine blunted LVH at 2 wk but not after 4 wk. Levels of AM and ANP gene expression increased as LVH developed but were completely suppressed by candesartan over 6 wk. ANP expression level was also attenuated by manidipine over 6 wk, whereas AM expression level was suppressed at 2 wk but not after 4 wk by manidipine. We concluded that diastolic WS and ANG II might be potent stimuli for the LVH and LV AM and ANP gene expression in volume overload and that diastolic WS could be relatively involved in the early LVH and in the gene expression of ANP rather than of AM.

Adrenomedullin↗

Enhanced adrenomedullin production by mechanical stretching in cultured rat cardiomyocytes.

Adrenomedullin (AM) is secreted from cultured cardiac myocytes. In this study, we examined whether mechanical stretching stimulates AM production in cardiac myocytes, and if so, whether angiotensin II (Ang II) is involved in that mechanism. Neonatal rat cardiac myocytes cultured in serum-free medium were stretched 10% or 20% on flexible silicone rubber culture dishes, and AM mRNA expression was examined by quantitative polymerase chain reaction. The AM mRNA levels in the myocytes stretched 10% and 20% for 24 hours significantly increased by 56% (P<0.05) and 88% (P<0.01), respectively, when compared with the levels in nonstretched cells. AM secretion into the medium after the myocytes were stretched 10% and 20% increased by 22% (P<0.05) and 45% (P<0.01), respectively. In nonstretched myocytes incubated with 10(-6) mol/L Ang II for 24 hours, AM mRNA and secretion increased by 86% (P<0.05) and 36% (P<0. 01), respectively. These effects of Ang II were abolished by 10(-6) mol/L CV-11974, an Ang II type I (AT(1)) receptor antagonist, but not by 10(-6) mol/L PD-123319, an Ang II type II antagonist. Stretch-induced increases of AM gene expression and secretion were significantly inhibited (P<0.05) in the presence of 10(-6) mol/L CV-11974 by 46% and 52%, respectively; however, they were not affected by 10(-6) mol/L PD-123319. These findings indicate that AM production from cardiac myocytes is augmented by mechanical stretching, partially through the AT(1) receptors, which suggests a local interaction between AM and the renin-angiotensin system in stretched cardiac myocytes.

Adrenomedullin↗

Angiographic coronary morphology in patients with ischemic heart disease.

OBJECTIVES: To determine whether ischemia- or infarct-related arteries (IRAs) are accompanied by certain findings specific to clinical settings, coronary cineangiography was reviewed of 71 patients with stable effort angina pectoris (SAP), 72 with unstable angina pectoris (UAP), 118 with acute myocardial infarction (AMI) and 137 with old myocardial infarction (OMI). METHODS: The morphology of identifiable ischemia- or infarct-related lesions (IRLs) was classified as totally occlusive, and simple (Type I lesion) or complex (Type II lesion). Complex lesions were subdivided into Type IIa lesions (narrowing with irregular, poorly defined or hazy borders, sharp leading or trailing edges that overhang or are perpendicular to vessel walls, and globular endoluminal negative images), Type IIb (2 or more serial, closely spaced narrowings together with multiple irregularities), Type IIc (luminal narrowing with extraluminal contrast pooling, single or paired short thin linear radiolucencies with or without a variable degree of outpouching, and narrowing with definite outpouching with or without radiolucency), and Type IId (narrowing with morphology not included in Types IIa-IIc). RESULTS: Total occlusive lesions among identifiable IRLs occurred at 17 sites (23.9%) in patients with SAP, 7 (9.7%) with UAP, 48 (40.7%) with AMI and 30 (21.9%) with OMI. The mean diameter stenosis of identifiable IRLs was 89.4% in patients with SAP, 92.0% with UAP, 93.1% with AMI, and 87.4% with OMI. Patent identifiable IRLs in patients with SAP had a significantly higher frequency of Type I lesions (29 sites, 40.8%) compared with those with UAP, AMI and OMI (p < 0.01), followed by a relatively lower occurrence of Types IIa 12 (16.9%), IIb 8 (11.3%), IIc 3 (4.2%) and IId 2 (2.9%) lesions. Patients with UAP were characterized by a higher occurrence of Type IIa (34 sites, 47.2%, p < 0.01) and IIc (13 sites, 18.1%, p < 0.01) lesions compared with those with SAP. Patients with AMI had total occlusion (48 sites, 40.7%, p < 0.05) and Type IIa lesion (38 sites, 32.2%, p < 0.05) more frequently than those with SAP. Patients with OMI showed fewer total occlusions (30 sites, 21.9%), same occurrence of Type IIa lesion (39 sites, 28.5%), and higher occurrence of IIb (23 sites, 16.8%) and IIc (20 sites, 14.6%) than those with AMI. CONCLUSIONS: This analysis of coronary cineangiographies from patients with UAP, AMI and OMI, which share a common pathogenesis, shows that IRAs, especially IRLs, are associated with certain morphology specific to clinical settings, and that the morphology and severity of stenosis could change in a short period. The present results may improve coronary cineangiography interpretation about pathophysiological issues in vivo affecting coronary circulation.

Adult↗

Differential hormonal profiles of adrenomedullin and proadrenomedullin N-terminal 20 peptide in patients with heart failure and effect of treatment on their plasma levels.

BACKGROUND: Adrenomedullin (AM) is a potent vasodilatory peptide discovered in human pheochromocytoma tissue. Proadrenomedullin N-terminal 20 peptide (PAMP) processed from an AM precursor is also a novel hypotensive peptide which inhibits catecholamine secretion from sympathetic nerve endings. HYPOTHESIS: The present study sought to examine the relationships between the two peptides and other clinical parameters by measuring the plasma AM and PAMP concentrations in 98 patients with heart failure. METHODS: In all, 98 patients [65 men and 33 women, aged 58.2 +/- 11.0 years, mean +/- standard deviation (SD)] with heart failure and 26 healthy volunteers (12 men and 14 women, aged 54.1 +/- 8.6 years) were examined in this study. Heart failure was secondary to previous myocardial infarction in 58 patients, valvular disease in 28, cardiomyopathy in 9, and congenital heart disease in 3. All patients were classified into two groups of class I or II (Group 1) and class III or IV (Group 2) according to the New York Heart Association (NYHA) functional classification. RESULTS: Both plasma AM and PAMP concentrations in the patients were significantly higher than those in healthy volunteers. In addition, plasma AM and PAMP concentrations in patients in class III or IV of New York Heart Association (NYHA) classification were significantly higher than those in NYHA class I or II. The elevated plasma concentrations of these peptides in patients in NYHA class III or IV significantly decreased in response to the treatment for 7 days. There was a significant correlation between plasma AM and PAMP, though the plasma concentration of PAMP was one-fifth to one-seventh of that of AM in patients and controls. The plasma AM concentration correlated significantly with the plasma concentrations of atrial and brain natriuretic peptides, epinephrine, and right atrial pressure, whereas such a relationship was not noted for the plasma PAMP concentration. CONCLUSIONS: Judging from the difference in not only the biological actions but also the hormonal profiles between AM and PAMP, they may differentially modulate the cardiovascular system in patients with heart failure, although they are processed from the same precursor.

Adrenomedullin↗

An autocrine or a paracrine role of adrenomedullin in modulating cardiac fibroblast growth.

OBJECTIVE: The aim of the present study was to determine the role of adrenomedullin (AM) in cardiac fibroblasts. METHODS: The production and secretion of AM were examined in cultured neonatal rat cardiac fibroblasts, and the effects of AM on proliferation and protein synthesis of these cells were assessed by [3H]thymidine and [3H]phenylalanine incorporation, respectively. RESULTS: Cultured cardiac fibroblasts secreted AM into the medium time-dependently at a rate of 20.3 +/- 3.0 fmol/5 x 10(4) cells/48 h, mean +/- S.D. Northern blot analysis showed expression of preproAM mRNA of 1.6 kb in these cells. In addition, 10(-6) mol/l of angiotensin II (Ang II) and endothelin-1 (ET-1) significantly increased the AM secretion by 55 and 48%, respectively. Synthetic AM significantly reduced 10(-6) mol/l Ang II- or 10(-7) mol/l ET-1-stimulated [3H]thymidine and [3H]phenylalanine incorporation in a dose-dependent manner, and these effects were attenuated by a calcitonin gene-related peptide (CGRP) type 1 receptor antagonist, CGRP(8-37). Synthetic AM also had a dose-dependent stimulatory effect on cAMP accumulation in these cells, which was significantly attenuated by CGRP(8-37). A cAMP analogue, 8-bromo-cAMP, mimicked the AM effects, inhibiting the Ang II-stimulated [3H]thymidine and [3H]phenylalanine incorporation. Blockage of the effect of endogenous AM by anti-AM monoclonal antibody not only significantly reduced the basal level of intracellular cAMP, but also enhanced the [3H]thymidine and [3H]phenylalanine incorporation into the cells. CONCLUSIONS: Cultured neonatal rat cardiac fibroblasts produce and secrete AM, and the secreted AM may inhibit proliferation and protein synthesis of these cells. AM may exert these inhibitory effects partly by elevating intracellular cAMP. It is suggested that AM has an important role in modulating the growth of cardiac fibroblasts in an autocrine or a paracrine manner.

8-Bromo Cyclic Adenosine Monophosphate↗

Secretion and clearance of the mature form of adrenomedullin in humans.

In the biosynthesis of adrenomedullin (AM), glycine-extended AM, an intermediate form (iAM) processed from proAM is converted to AM[1-52]-NH2, the bioactive mature form of AM (mAM), by enzymatic amidation. We earlier showed that both molecular forms of AM circulate in human plasma. In the present study, to investigate the secretion and clearance sites of mAM and iAM in humans, we examined the plasma mAM and iAM concentrations in the femoral artery and vein (FA and FV), the aortic root and coronary sinus (AO and CS), and the pulmonary artery and capillary (PA and PC) of patients with ischemic heart disease. Plasma mAM in FV was significantly (p<0.001) higher than in FA. There also was a significant (p<0.001) step-up in the plasma mAM of the CS as compared to the AO. In contrast, plasma mAM was significantly (p<0.001) reduced in the PC as compared to the PA. However, such differences were not observed in plasma iAM levels. These findings suggest that in humans the vasculature of the lower extremities and the heart produce and secrete mAM and that the lung is a clearance site of circulating mAM.

Adrenomedullin↗

Molecular forms of circulating adrenomedullin in patients with congestive heart failure.

In the biosynthesis of adrenomedullin (AM), an intermediate form, AM(1-52)-glycine-COOH (iAM), is cleaved from proAM and subsequently processed to a biologically active mature form, AM(1-52)-NH2 (mAM), by enzymatic amidation. We recently reported that immunoreactive AM in human plasma consists of mAM and iAM. To clarify the pathophysiological roles of mAM and iAM in heart failure, we established an assay method to specifically detect mAM, and we determined the plasma concentrations of mAM and iAM in 68 patients with congestive heart failure (CHF). The plasma mAM concentrations of the CHF patients classified as being class I or II of New York Heart Association (NYHA) functional classification were significantly greater than those of the 28 healthy controls, and a further increase was noted in the class III or IV patients. Similar increases in plasma iAM were also observed in these patients compared with controls. The increased plasma mAM and iAM in 12 patients with exacerbated CHF were significantly reduced by treatment of their CHF for 7 days. In addition, the plasma concentrations of both mAM and iAM were significantly correlated with pulmonary capillary wedge pressure, pulmonary artery pressure, right atrial pressure, cardiothoracic ratio, heart rate, and the plasma concentrations of atrial and brain natriuretic peptides in the CHF patients. Thus the plasma concentrations of both mAM and iAM were increased progressively in proportion to the severity of CHF. These results suggest that, though the role of iAM remains to be clarified, mAM acts against the further deterioration of heart failure in patients with CHF.

Adrenomedullin↗

[One-hour protocol stress myocardial scintigraphy: prospective study of diagnostic accuracy for the detection of coronary artery stenosis].

A one-hour protocol for stress myocardial scintigraphy using technetium-99m-tetrofosmin (Tc-tetrofosmin) was compared with coronary arteriography for the detection of coronary artery stenosis in 90 consecutive patients without prior myocardial infarction, revascularization procedure or vasospastic angina. Tc-tetrofosmin stress myocardial scintigraphy acquired a rest image 20 min after intravenous administration of Tc-tetrofosmin (185 MBq, 1/5 vial) using a three-head gamma camera collecting 20-sec views over 360 degrees. The stress test using bicycle ergometer was performed and administration of Tc-tetrofosmin (740 MBq, 4/5 vial) was repeated at the peak stress point. The stress image was acquired 15 min after the second injection with 5-sec views over 360 degrees. Coronary arteriography revealed the presence of significant coronary artery stenosis (> 75%) in 56 vessels of 45 patients, including 35 patients with single-vessel disease, 5 with two-vessel disease, 2 with three-vessel disease, and 3 with left main trunk disease. The overall sensitivity and specificity for the detection of coronary artery disease by visual analysis were 91.1% and 77.8%, respectively, and by quantitative analyses (using bull's-eye method) were 95.6% and 91.1%, respectively. The individual stenotic vessel sensitivities in the right coronary artery, left anterior descending artery, and left circumflex artery were 84.6%, 90.9%, and 78.6%, respectively. The specificities were 97.3%, 95.9%, and 100.0%, respectively. These results suggest that stress myocardial scintigraphy using the present new protocol is a promising approach for the detection of coronary artery stenosis.

Angina Pectoris↗

Disappearance of complete atrioventricular block after chemotherapy for malignant lymphoma: a case report.

A 77-year-old man with malignant lymphoma presented with dizziness and exertional dyspnea. Physical examination revealed marked bradycardia (36 beats/min). Twelve-lead electrocardiography showed complete atrioventricular block with narrow QRS escape beats. Gallium scintigraphy demonstrated significant abnormal uptake in the heart. Transesophageal echocardiography showed a thick interatrial septum with increased echogenecity. He underwent chemotherapy under external temporary pacing with a suspected diagnosis of complete atrioventricular block secondary to cardiac invasion of malignant lymphoma. Atrioventricular conduction progressively improved and the complete atrioventricular block disappeared. He is currently well and has required no cardiac pacing for 6 months. We conclude that complete atrioventricular block may be reversible in some patients with malignant lymphoma, even in the elderly.

Aged↗