Magnesium deficiency in patients with recent myocardial infarction and provoked coronary artery spasm. (49/422)

This study sought to clarify the relationship between magnesium (Mg) deficiency and coronary artery spasm provoked by pharmacologic agents in patients with a recent acute myocardial infarction (AMI). Twenty-three consecutive patients suffering from AMI were investigated with a Mg retention test (Mg: 0.1 mmol/kg for 4 h) in both the acute phase (within I week (3+/-2 days) of onset) and the subacute phase (3-4 weeks (24+/-6 days) of the onset). Early coronary arteriography was performed in all patients. Coronary stenosis in the infarct-related artery was less than 90% in all patients in the subacute phase. The spasm provocation test was performed in the subacute phase and coronary spasm was defined as transient subtotal or total occlusion in association with angina or electrocardiographic ST-segment deviation. Coronary artery spasm was provoked in only 13 of the 23 patients. Compared with the control subjects (12 patients without coronary artery disease or coronary spasm), the 24-h Mg retention was significantly higher in patients with AMI (acute phase: 78+/-27%, subacute phase: 66+/-32%, vs control: 48+/-12%, p<0.05). In the subacute phase, the 24-h Mg retention decreased in patients without coronary spasm (43+/-26%), but a high level of Mg retention was still observed in patients with coronary spasm (84+/-25%). There was no difference in the serum concentrations of Mg, calcium and phosphorus between the 2 groups on both phases. In conclusion, both Mg deficiency and provoked coronary artery spasm were noted in more than half of the Japanese patients with a recent AMI, suggesting a close association between Mg deficiency and AMI.  (+info)

Progesterone regulation of vascular thromboxane A(2) receptors in rhesus monkeys. (50/422)

We hypothesized that progesterone regulates thromboxane A(2) receptor (TxA(2)R) density in primate vascular muscle and that TxA(2)R density correlates with coronary reactivity in vivo and in vitro. Reactivity to serotonin + U-46619 was determined by angiography in surgically postmenopausal [ovariectomized (Ovx)] rhesus monkeys without progesterone replacement and after 2-wk progesterone treatment (1-2 ng/ml). In untreated Ovx animals, 100 micromol/l serotonin + 1 micromol/l U-46619 (syringe concentrations) provoked vasospasm-like constrictions in six of six monkeys; zero of six progesterone-treated monkeys developed vasospasms. Sustained Ca(2+) responses in vascular muscle cells isolated from Ovx coronaries (208 +/- 63% of basal 20 min after stimulation) treated with serotonin + U-46619 contrasted with transient Ca(2+) responses (143 +/- 18% of basal and decreasing 5 min after stimulation) in progesterone-treated monkeys. The maximum density of [1S-(1I,2J(5Z),3I(1E,3R*),4I)]-7-[3-(3-hydroxy-4-(4'-[(125)I]iodophenoxy)- 1-butenyl)-7-oxabicyclo[2.2.1]heptan-2-yl]-5-heptenoic acid ([(125)I]-BOP) binding was greater (P < 0.01) in carotid arteries and aortic membranes from Ovx (109 +/- 11 fmol/mg) compared with progesterone-treated (43 +/- 15 fmol/mg) monkeys. TxA(2)R immunolabeling revealed greater coronary TxA(2)R labeling in Ovx compared with progesterone-treated monkeys. The results suggest that progesterone can decrease arterial TxA(2)R in Ovx monkeys.  (+info)

Clinical and angiographic effects of chronic calcium channel blocker therapy continued beyond first postoperative year in patients with radial artery grafts: results of a prospective randomized investigation. (51/422)

BACKGROUND: This study was conceived to elucidate the clinical and angiographic effects of chronic calcium channel blocker therapy (CCCBT) continued after the first postoperative year in patients in whom the radial artery (RA) was used for myocardial revascularization. METHODS AND RESULTS: Patients who received RA grafts at our institution and who at 1 year had no scintigraphic evidence of ischemia in the RA territory or angiographic evidence of RA malfunction (n=120) were randomly assigned to continue (n=63) or suspend (n=57) the CCCBT with diltiazem (120 mg/d). After 5 years, all patients were reassessed clinically and by stress myocardial scintigraphy, and 87 of them (45 from the continued group that continued CCCBT and 42 from the group that suspended CCCBT) were restudied angiographically. No differences regarding either the clinical and scintigraphic results or the RA angiographic status were demonstrated between the 2 groups. CONCLUSIONS: After the first postoperative year, the continuation of CCCBT does not affect RA graft patency or clinical and scintigraphic results.  (+info)

Antiischemic properties of fasudil in experimental models of vasospastic angina. (52/422)

We studied the antiischemic properties of fasudil, a Rho-kinase inhibitor, in conscious rabbits with coronary vasospasm induced by vasopressin and endothelin. Pretreatment with fasudil (0.3 and 3 mg/kg) attenuated the maximum elevation of the T-wave elicited by endothelin. Pretreatment with fasudil inhibited the T-wave elevation elicited by vasopressin. Fasudil and hydroxy fasudil, an active metabolite of fasudil, relaxed the endothelin-, U-46619-, 5-hydroxytryptamine- or histamine-induced contraction in swine coronary arterial strips. Fasudil and hydroxy fasudil significantly prevented the reduction in coronary flow by vasopressin in the Langendorff perfused rat heart. Fasudil was effective in protecting the heart against vasopressin and endothelin-induced myocardial ischemic change in conscious rabbits, and this beneficial effect can be attributed to its action of ameliorating the severe contraction of arteries. The inhibition of Rho-kinase may have implications for the development of novel therapeutic strategies for vasospastic angina in patients.  (+info)

Coronary vasospasm inducing dynamic left ventricular outflow tract obstruction. (53/422)

An 80-year-old man was admitted to the emergency department of our institution due to acute, anterior-wall myocardial infarction and cardiogenic shock. Two-dimensional echocardiography revealed systolic anterior motion of the mitral leaflets with severe left ventricular outflow tract obstruction. Although coronary angiography showed normal coronary arteries, an ergonovine provocation test induced diffuse coronary constriction of the left coronary artery, with chest pain, and ST-T changes seen on the electrocardiogram. These clinical signs caused us to suspect coronary spasm. The present case serves as a reminder that coronary vasospasm may be a factor in the development of dynamic left ventricular outflow tract obstruction. Early detection and intensive efforts to relieve vasospasm, including emergency coronary angiography and intracoronary injection of nitroglycerin, are essential.  (+info)

Coronary artery endothelial protection after local delivery of 17beta-estradiol during balloon angioplasty in a porcine model: a potential new pharmacologic approach to improve endothelial function. (54/422)

OBJECTIVES: The goal of this research was to study the effect of locally delivered 17beta-estradiol (17beta-E) during angioplasty on endothelial function after percutaneous transluminal coronary angioplasty (PTCA) at four weeks. BACKGROUND: The endothelium plays a major role in the structural and functional integrity of coronary arteries and is damaged by PTCA. METHODS: Juvenile swine were subjected to PTCA, after which each artery was randomly-assigned to 600-microg 17beta-E delivered locally, an equal volume of vehicle (V) or PTCA alone. After four weeks, the improvement in endothelial function was assessed by angiography using intracoronary acetylcholine (Ach) infusion and by immunohistochemistry. RESULTS: At 10(-5) mol/l and 10(-4) mol/l Ach, significant vasoconstriction was noted in arteries treated with PTCA alone (p < 0.01 and p < 0.0001, respectively) and with PTCA plus V (p < 0.02 and p < 0.001, respectively). No significant vasoconstrictive response to Ach was observed in arteries treated with PTCA plus 17beta-E. Immunohistochemistry of vessels four weeks after PTCA revealed enhanced re-endothelialization (p < 0.0005) and endothelial nitric-oxide synthase (eNOS) expression (p < 0.0005) in PTCA plus 17beta-E-treated arteries compared with the other two treatment groups. Arteries treated with 17beta-E showed significantly lower neointima formation, which correlated inversely with the extent of re-endothelialization and eNOS expression. CONCLUSIONS: Locally delivered 17beta-E significantly enhances re-endothelialization and endothelial function after PTCA, possibly by improving the expression of eNOS. Since endothelial dysfunction can promote both restenosis and coronary spasm, local 17beta-E administration is a promising new approach to improve long-term results after PTCA.  (+info)

5-fluorouracil-induced cardiotoxicity mimicking myocardial infarction: a case report. (55/422)

BACKGROUND: Severe cardiotoxicity is a documented, but very unusual side-effect of intravenous 5-fluorouracil therapy. The mechanism producing cardiotoxicity is poorly understood. CASE PRESENTATION: A case of 5-fluorouracil-induced cardiotoxicity, possibly due to coronary artery spasm, and mimicking acute anterolateral myocardial infarction is presented and discussed. Electrocardiographs highlighting the severity of the presentation are included in the report along with coronary angiograms demonstrating the absence of significant coronary atherosclerosis. CONCLUSION: Severe 5-fluorouracil-induced cardiotoxicity is rare, but can be severe and may mimic acute myocardial infarction, leading to diagnostic and therapeutic dilemmas. Readministration of 5-fluorouracil is not advised following an episode of cardiotoxicity.  (+info)

Significance of reduced uptake of iodinated fatty acid analogue for the evaluation of patients with acute chest pain. (56/422)

OBJECTIVES: To assess whether 15-(p-[iodine-123] iodophenyl)-3-(R,S) methylpentadecanoic acid (BMIPP) imaging can identify previous ischemic areas, BMIPP SPECT was performed in patients with acute chest pain to compare its findings with those of technetium-99m-tetrofosmin (tetrofosmin) SPECT and coronary angiography. BACKGROUND: Basic studies indicate that BMIPP can identify previous ischemia as reduced tracer uptake. METHODS: This study prospectively enrolled 111 consecutive patients with acute chest pain without myocardial infarction. Tetrofosmin SPECT was performed at rest within 24 h after the last episode of chest pain. Coronary angiography and BMIPP SPECT were also performed on the following day. RESULTS: Sixty-four of the 87 patients with coronary stenosis or spasm showed BMIPP abnormalities corresponding to the areas of coronary abnormalities (sensitivity 74%), whereas only 33 of them showed perfusion abnormalities (sensitivity 38%) (p < 0.001). Of 24 patients [corrected] without coronary stenosis or spasm, 22 showed normal BMIPP SPECT (specificity = 92%) [corrected] and 23 showed normal tetrofosmin SPECT (sensitivity = 96%) [corrected]. Coronary stenosis was more often seen in the group with abnormal tetrofosmin/abnormal BMIPP (82%) and with normal tetrofosmin/abnormal BMIPP (69%) than in the group with normal tetrofosmin/normal BMIPP (36%) (p < 0.05). Coronary spasm was observed more often in the group with abnormal tetrofosmin/abnormal BMIPP (83%) and with normal tetrofosmin/abnormal BMIPP (90%) than in the group with normal tetrofosmin/normal BMIPP (27%) (p < 0.05). The extent and severity scores of tetrofosmin and BMIPP in the patients with organic stenosis were significantly higher than those of patients with no organic stenosis or spasm (p < 0.0001). CONCLUSIONS: These data indicate that BMIPP SPECT may specifically identify previous ischemic lesions due to coronary stenosis or spasm in patients with acute chest pain.  (+info)