Arteries within the artery of coronary artery in an adult patient with acute coronary syndrome.

A 40-year-old man with acute coronary syndrome underwent coronary angiography, which showed a somewhat irregular contour with radiolucent lines in the left anterior descending artery. Intravascular ultrasound disclosed that the arterial lumen was separated by confining walls, yielding multiple inner lumens. Implantation of drug eluting stents resulted in slow coronary run-off, which was restored soon after intra-aortic balloon pumping support. The multiple inner lumens correspond to the histopathological finding of "arteries within the artery". While "arteries within the artery" is seen exclusively in children with a history of Kawasaki disease, it is rare in adults with undiagnosed Kawasaki disease.

Differential effects of calcium-channel blockers on vascular endothelial function in patients with coronary spastic angina.

BACKGROUND: The effects of the 3 classes of L-type calcium-channel blockers (CCBs) on vascular endothelial function have not been clarified in patients with coronary vasospasm. METHODS AND RESULTS: Twenty-five normotensive patients (age 64.0+/-1.4 years) with coronary vasospasm were randomly treated for 3 months with benidipine, diltiazem, and verapamil, which belong to the dihydropyridine, benzothiazepine, and phenylalkylamine classes of CCBs, respectively. Endothelium-dependent flow-mediated dilatation (FMD), endothelium-independent nitroglycerin-induced dilatation in the brachial arteries, and plasma cyclic guanosine 3',5'-monophosphate (cGMP), a nitric-oxide-related product, were assessed before and after treatment. At baseline, the patients with vasospasm had significantly lower FMD as compared with normal subjects (n=8). Blood pressure did not differ among the 3 groups before and after treatment. Benidipine significantly increased FMD (from 4.7+/-0.6 to 7.4+/-1.1%, P<0.05) and plasma cGMP levels. In contrast, neither diltiazem nor verapamil affected FMD and cGMP levels. None of the treatments affected nitroglycerin-induced dilatation. CONCLUSIONS: Benidipine, but not diltiazem or verapamil, improves endothelial dysfunction beyond blood pressure lowering effects in patients with coronary vasospasm. Upregulation of the nitric oxide - cGMP system by benidipine may partly contribute to the improvement. The dihydropyridine class may be more beneficial for vascular endothelial function than the non-dihydropyridine classes of CCBs.

Neurogenic stunned myocardium associated with status epileptics and postictal catecholamine surge.

A 75-year-old woman developed left ventricular apical ballooning, shortly after recovering from status epileptics. Plasma noradrenaline and adrenaline levels were 2.05 ng/ml and 0.48 ng/ml, respectively. Endomyocardial biopsy disclosed patchy areas of interstitial myocardial fibrosis, atrophy and vacuolization of cardiac myocytes, and some disappearance of myocyte nuclei. Follow-up echocardiography showed that the left ventricular apical ballooning was restored to normal within 25 days. These findings are compatible with neurogenic stunned myocardium. It is important to recognize that patients suffering from intractable seizures may harbor a risk of postictal catecholamine surge and catecholamine-induced myocardial dysfunction.

Vitamin C restores the contractile response to dobutamine and improves myocardial efficiency in patients with heart failure after anterior myocardial infarction.

BACKGROUND: Excessive oxidative stress is considered one of the mechanisms of a decrease in contractile force without concomitant reduction in oxygen cost in failing myocardium. We hypothesized that the antioxidant vitamin C may help reverse hyporesponsiveness to beta-adrenergic stimulation and improve myocardial efficiency in patients with heart failure (HF) after myocardial infarction (MI). METHODS AND RESULTS: Nineteen patients with mild to moderate HF due to previous MI (mean left ventricular [LV] ejection fraction 39%) were instrumented with conductance and coronary sinus thermodilution catheters. Left ventricular contractility, expressed as E(es), the slope of end-systolic pressure-volume relationship, and mechanical efficiency, expressed as the ratio of LV stroke work (SW) to myocardial oxygen consumption (MVO2), were measured in response to the intravenous infusion of dobutamine (4 microg/kg per min) before (Dob) and during (Dob + Vit C) the infusion of vitamin C (2.0-g bolus injection and subsequent 50-mg/min infusion through the jugular vein) (vitamin C group, n = 10). The infusion of vitamin C augmented the E(es) response to dobutamine by 20% +/- 8% (Dob 2.1 +/- 0.3, Dob + Vit C 2.5 +/- 0.4 mm Hg/mL, P < .01) and the SW/MVO2 response by 21% +/- 5% (Dob 36% +/- 3%, Dob + Vit C 43% +/- 4%, P < .01). In the control group (n = 9), E(es) and SW/MVO2 were measured in response to dobutamine before (Dob) and during (Dob + vehicle) the infusion of saline. No difference in E(es) or SW/MVO2 was observed between Dob and Dob + vehicle (E(es): Dob 2.1 +/- 0.2, Dob + vehicle 2.1 +/- 0.2 mm Hg/mL per square meter, P = nonsignificant) (SW/MVO2: Dob 35% +/- 4%, Dob + vehicle 33% +/- 4%, P = nonsignificant). CONCLUSION: The administration of the antioxidant vitamin C enhances the contractile response to dobutamine and improves myocardial efficiency in patients with HF.

Inhibition of endogenous nitric oxide synthase augments contractile response to adenylyl cyclase stimulation without altering mechanical efficiency in patients with idiopathic dilated cardiomyopathy.

BACKGROUND: Increased nitric oxide (NO) in the failing heart attenuates the myocardial contractile response to beta-adrenergic receptor stimulation. However, the physiological effects of NO on the beta-adrenergic post-receptor signaling system are unknown. The objective of the present study was to examine the effects of cardiac NO synthase (NOS) inhibition on left ventricular (LV) hemodynamics and mechanoenergetics in response to adenylyl cyclase stimulation in human heart failure. METHODS AND RESULTS: The study group comprised 13 patients with heart failure because of idiopathic cardiomyopathy (IDC). Emax was examined as an index of LV contractility, LV external work (EW), pressure-volume area (PVA), myocardial oxygen consumption (MVO2), and mechanical efficiency (EW/MVO2) with the use of conductance and coronary sinus thermodilution catheters before and during colforsin daropate infusion, and during concurrent infusion of colforsin daropate with the NOS inhibitor, NG-monomethyl-L-arginine (L-NMMA; 200 micromol). Colforsin daropate increased Emax by 53% and EW by 18%, and reduced PVA by 14%, without altering MVO2 or mechanical efficiency. The combination of colforsin daropate with L-NMMA further increased Emax by 26% and reduced PVA by 9%, without altering MVO2 or mechanical efficiency. CONCLUSIONS: These findings suggest endogenous NO may modulate beta-adrenergic post-receptor pathways and preserve myocardial efficiency in patients with IDC.

Occult gastrointestinal bleeding due to acquired von Willebrand syndrome in a patient with hypertrophic obstructive cardiomyopathy.

A 69-year-old woman presented with a harsh systolic murmur and severe anemia. Echocardiography demonstrated hypertrophic obstructive cardiomyopathy with a peak pressure gradient of 154 mmHg. Endoscopic examinations disclosed an angiodysplasia and multiple diverticula in the colon, but no active bleeding was noted in these lesions. A selective defect of large multimers of von Willebrand factor was detected by electrophoresis. After collection of anemia and Ca antagonist therapy, left ventricular obstruction was relieved and cessation of the occult gastrointestinal bleeding was obtained. This is the first report whereby acquired type 2A von Willebrand syndrome was caused by hypertrophic obstructive cardiomyopathy.

Sumatriptan provokes coronary artery spasm in patients with variant angina: possible involvement of serotonin 1B receptor.

BACKGROUND: Serotonin (5HT) can induce coronary artery spasm (CAS) in patients with variant angina (VA). We have previously reported that 5HT(1B) and 5HT(2A) receptors gene were expressed in human coronary arterial smooth muscle cells and that isolated coronary artery from a patient with VA showed the supersensitivity to sumatriptan (SMT), a 5HT(1B/1D) receptor agonist. The aim of the present study was to determine whether SMT can provoke CAS directly or indirectly through platelet aggregation in patients with VA. METHODS: We evaluated the effects of intracoronary infusion of graded concentrations of SMT on coronary arteries in 9 patients, including 5 documented VA and 4 participants with atypical chest pain as control. RESULTS: SMT provoked CAS in all patients with VA. SMT could not induce CAS in control. SMT (10(-4) M) caused significant contractions (%diameter of baseline; median [interquartile range], 0 [0-18.4]% in VA, as compared with control (proximal segments; 92.6 [77.9-118.9]%, p<0.05 vs. VA, distal segments; 92.9 [65.3-158.5]%, p<0.01 vs. VA). In control, minor dilation occurred at SMT concentration up to 10(-5) M. SMT could induce in vitro platelet aggregation neither in healthy subjects nor in patients with VA. CONCLUSIONS: These findings suggest that activation of 5HT(1B) receptor by SMT can induce CAS directly in patients with VA without platelet activation. This is the first report directly demonstrating the effect of 5HT(1B) receptor activation on human coronary arteries in vivo.

[Recurrent episodes of takotsubo-like transient left ventricular ballooning occurring in different regions: a case report].

A 62-year-old male with emphysema developed recurrent episodes of transient left ventricular ballooning occurring in different regions. Left ventriculography revealed symmetric mid-ventricular ballooning when he was 60 years old, and he also developed mid-ventricular ballooning of larger extent at the age of 62 years. Furthermore, as he was treated for severe asthma attack 3 months later, left ventricular apical ballooning occurred. Echocardiography also demonstrated akinetic wall motion in the right ventricular apex. These episodes showed myocardial infarction-like onset, ST elevations on electrocardiography, no significant increases in cardiac enzymes, wall motion abnormalities incompatible with coronary artery disease, and complete recovery within a few weeks. From these findings, we speculate that the recurrent left ventricular wall motion abnormalities including the mid-ventricular ballooning were so-called takotsubo-like left ventricular dysfunction.

Recurrent severe mitral regurgitation due to left ventricular apical wall motion abnormality caused by coronary vasospastic angina: a case report.

A 76-year-old man developed congestive heart failure due to severe mitral regurgitation after episodes of vasospastic angina. Echocardiography demonstrated left ventricular apical akinesis with ballooning and deformity of the anterior mitral leaflet becoming concave toward the left atrium. The acetylcholine provocation test induced diffuse coronary vasospasm in the distal segments of both right and left coronary arteries and reproduced severe mitral regurgitation. Follow-up echocardiography demonstrated decreased mitral regurgitation with ameliorated apical wall motion. Coronary vasospasm remained refractory to antivasospastic medications and severe mitral regurgitation relapsed 1 month after discharge. Mitral valve annuloplasty with a Carpentier-Edwards physio ring was performed, and no recurrence of mitral regurgitation was observed despite some episodes of vasospastic angina. We speculate that vasospastic angina and the resultant apical wall motion abnormality caused tethering of the mitral subvalvular apparatus, leading to inappropriate mitral coaptation and severe regurgitation.

Depletion of antioxidants is associated with no-reflow phenomenon in acute myocardial infarction.

BACKGROUND: No-reflow phenomenon is observed in approximately one-third of patients after percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI), and is associated with poor functional and clinical outcomes. On the other hand, the formation of free radicals in vasculature exerts deleterious effects on coronary microcirculation. HYPOTHESIS: We hypothesized that redox state in coronary circulation may play a crucial role in no-reflow phenomenon in AMI. METHODS: Consecutive 26 patients with first AMI who underwent primary PCI < 24 h after onset were enrolled. Before PCI, blood samples were obtained from coronary sinus to measure plasma or serum antioxidative vitamins (vitamin C, vitamin E, and beta-carotene) and antioxidative enzymes (extracellular glutathione peroxidase [GPX], superoxide dismutase, and catalase). After PCI, the corrected Thrombolysis In Myocardial Infarction (TIMI) frame count (CTFC) was measured in the target vessel. Patients with TIMI < or = 2 flow despite an optimal PCI result were designated as no-reflow group (Group NR, n = 6) and the others as reflow group (Group R, n = 20). RESULTS: Levels of vitamin C, vitamin E, and GPX before PCI were significantly lower in Group NR than in Group R. The CTFC correlated inversely with levels of vitamin C, vitamin E, and GPX (p < 0.05). CONCLUSIONS: Depletion of antioxidants is associated with no-reflow phenomenon in AMI. These findings strongly suggest that the redox state in coronary circulation plays an important role in the pathogenesis of no-reflow phenomenon.