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A recent study revealed that recurrence of myocarditis occurs in a significant proportion of patients, but multiple recurrences of myocarditis have rarely been reported. The pathophysiology and best treatments for multiple recurrences of myocarditis remain unclear. A 60-year-old man presented to our emergency department with fever and chest pain. Physical examination, imaging, and laboratory findings were consistent with fulminant myocarditis. Paired titers confirmed adenovirus infection. The patient was treated with intra-aortic balloon pump and percutaneous cardiopulmonary support for 7 days and was discharged with near-normal electrocardiographic and echocardiographic findings on day 26. Over the subsequent 3 years, the patient experienced six episodes of recurrence of myocarditis with a progressive decrease in his ability to perform activities of daily living. At the time of his sixth recurrence, he died of ventricular fibrillation. Autopsy revealed mild enlargement of the left ventricle, extensive inflammatory cell infiltration, and mild interstitial fibrosis, suggesting left ventricle remodeling because of repetitive myocarditis. We have presented a case of multiple recurrences of myocarditis. This is the largest number of recurrences in a single patient reported to date. Further studies are needed to elucidate the underlying pathogenesis and best treatment of this condition.

Mechanisms of acute myocardial infarction caused by traumatic coronary artery injury have been reported. However, late-onset coronary artery stenosis associated with trauma is less well known. We experienced a case in which acute myocardial infarction of the right coronary artery occurred at the time of blunt chest trauma (BCT) caused by a traffic accident and an increase in coronary artery stenosis in the left anterior descending artery (LAD) branch about 1 year later. A comparison of a volume-rendering image created from enhanced-contrast computed tomography at the time of trauma and coronary angiography revealed that the trauma site and the stenotic lesion in the LAD were in very close proximity, suggesting to us that traumatic coronary artery injury without flow limitation may have developed into high-grade stenosis in the LAD 1 year later. In this case we were able to demonstrate a causal relationship between BCT and delayed coronary artery stenosis. After BCT, it is necessary to be aware of the possibility of delayed coronary artery stenosis even if coronary injury is absent in the acute phase.

Background We evaluated the diagnostic value of resting echocardiographic findings including total heart calcification (THC) score in combination with dobutamine stress echocardiography (DSE) for detection of myocardial ischemia. Methods Altogether, 110 patients with suspected angina pectoris underwent resting echocardiography and DSE. On the basis of resting echocardiography, we determined the THC score, left anterior descending artery diastole-to-systole velocity ratio (LAD-DSVR), and positive myocardial velocity during isovolumic relaxation phase (VIVR) detected by color-coded tissue Doppler imaging. Myocardial ischemia was diagnosed by a 25% or greater reduction in the internal diameter of major coronary vessels with impaired fractional flow reserve (FFR ≤0.80). Results DSE had excellent specificity (89%) but modest sensitivity (52%) for wall-motion abnormality (WMA) analysis. Multivariate analysis showed that THC score ≥2 (odds ratio and 95% confidence interval: 4.49 [2.29–10.6]; P = 0.018), LAD-DSVR ≤1.5 (6.43 [1.39–20.3], P = 0.019), and duration of positive VIVR ≥71 msec (7.93 [3.72–12.1]; P

Background Aortic valve stenosis (AS) is characterized by chronic left ventricular pressure overload, leading to left ventricular hypertrophy (LVH). We assessed correlations in left ventricular volumes and function between echocardiography and quantitative gated SPECT (QGS) in patients with AS. Methods and results The study population consisted of 28 patients with AS defined as a peak velocity of > 3.0 m/s and 28 age- and sex-matched control subjects. Patients with AS had a peak pressure gradient of 73.4 ± 24.5 mm Hg and a larger LVM index compared to control subjects (115.5 ± 29.2 g/m2 vs 78.3 ± 12.1 g/m2, p

BackgroundBoth aortic aneurysms and coronary artery ectasia (CAE) frequently coexist and are associated with more pronounced inflammation. Neutrophil to lymphocyte ratio (NL ratio) is widely used as a marker of inflammation. However, relation between CAE and NL ratio in patients with aortic aneurysms is not fully understood. This study was undertaken to assess relation between CAE and NL ratio in patients with aortic aneurysms.MethodsThis study consisted of 93 consecutive patients with aortic aneurysms (AA group) and 79 patients without aortic aneurysms who had angiographically normal coronary arteries as the control group. Moreover, patients with aortic aneurysms were classified into two groups based on the presence of CAE; CAE (+) group (n = 44) and CAE (−) group (n = 49). We compared blood chemical parameters in both groups.ResultsIn the AA group, 44 patients (47.3%) had CAE. The AA group had a significantly higher NL ratio than the control group (2.93 ± 1.43 vs. 2.45 ± 1.05, p = 0.027). Furthermore, the CAE (+) group had a significantly higher NL ratio than the CAE (−) group (3.39 ± 1.67 vs. 2.52 ± 1.04, p < 0.01). Multivariate logistic regression analysis revealed that the high NL ratio was an independent predictor for CAE in patients with aortic aneurysms (odds ratio 1.76, 95% confidence interval 1.24–2.69, p = 0.001).ConclusionsPatients with aortic aneurysms had a significantly higher NL ratio than those without aortic aneurysms. Furthermore, the NL ratio might predict the presence of CAE in patients with aortic aneurysms.

Aortic aneurysms are associated with coronary artery ectasia (CAE). However, the relation between the extent of CAE and coronary blood flow in patients with aortic aneurysms is not fully understood. This study was undertaken to assess the angiographic characteristics and effects of the topographical extent of CAE on coronary blood flow in patients with aortic aneurysms. This study consisted of 93 consecutive patients with aortic aneurysms (AA group) and 79 patients without aortic aneurysms who had angiographically normal coronary arteries as the control group (Control group). Coronary flow velocity was determined using the thrombolysis in myocardial infarction frame count (TFC) and the topographical extent of CAE was assessed. In the AA group, 43 patients (46.2 %) had significant coronary artery stenosis and 37 patients (40.2 %) had diffuse CAE. TFC was significantly higher in the AA group than in the control group in all 3 coronary arteries. Furthermore, mean corrected TFC (CTFC) was significantly higher in the AA group than in the control group (40.1 ± 10.7 vs. 25.8 ± 6.5, p < 0.001). In the AA group, mean CTFC in patients with diffuse CAE was significantly higher than that in patients with segmental CAE (50.2 ± 8.7 vs. 33.6 ± 5.2, p < 0.001). The mean CTFC correlated positively with the topographical extent of CAE. Many patients with aortic aneurysms were accompanied with angiographic coronary artery stenosis and CAE. Furthermore, patients with aortic aneurysms had higher CTFC than those without aortic aneurysms and it was primarily driven by more frequent prevalence of diffuse CAE.

Heart Score View (HSV) is a free software package for automated quantification of myocardial single photon emission computed tomography (SPECT) imaging using a standard Windows computer. We compared scoring results of myocardial perfusion among visual analysis, Quantitative Perfusion SPECT (QPS), and HSV in patients with known or suspected coronary artery disease.This study included 75 consecutive patients with known or suspected coronary artery disease who underwent adenosive stress-rest Tl-201 SPECT. Analysis of myocardial perfusion SPECT was performed on a standard 17-segment model visually and using QPS and HSV.There were 54 male and 21 female patients with a mean age of 70.5 ± 10.7 years. Thirteen patients (17%) had prior myocardial infarction. Summed stress score (SSS) and summed rest score (SRS) in the mid and basal areas were significantly higher on HSV than visual analysis or QPS. There was no significant difference in SDS in the whole area among the 3 methods. Similar results were found even in patients without prior myocardial infarction. Manual setting of the left ventricular cavity improved the correlations of SSS, SRS and SDS between HSV and the other methods.Our data suggested that HSV was comparable with visual analysis or QPS in scoring myocardial perfusion when manual setting of the left ventricular cavity is applied.

Stent thrombosis remains a severe complication after deployment owing to its high mortality. In the current report, we present a case of stent thrombosis distal to the segment showing flow-limiting early in-stent restenosis with an everolimus-eluting stent.

Malondialdehyde-modified low-density lipoprotein (MDA-LDL) is considered to play an essential role in plaque destabilization. We aimed to investigate the association between the tissue characteristics of culprit plaque assessed by integrated backscatter (IB)-intravascular ultrasound (IVUS) and the serum MDA-LDL levels in patients with stable coronary artery disease.The study group consisted of 179 patients undergoing IB-IVUS during elective percutaneous coronary intervention. Patients were classified into 2 groups based on serum MDA-LDL level: low MDA-LDL group (102 U/L, n=88) and high MDA-LDL group (≥102 U/L, n=91). Plaques in the high MDA-LDL group had higher %lipid (45.2±12.5% vs. 54.9±14.5%, P0.001) and lower %fibrosis (43.0±9.1% vs. 36.4±11.4%, P0.001) than did plaques in the low MDA-LDL group. Lipid-rich plaque (%lipid60% or %fibrosis30%) was significantly more frequently found in the high MDA-LDL group than in the low MDA-LDL group (14.3% vs. 39.8%, P0.001). The incidence of MACE (cardiac death, myocardial infarction and/or hospitalization for heart failure) during 3 years was significantly higher in the high MDA-LDL group than in the low MDA-LDL group (6.6% vs. 15.9%, P=0.02).Higher MDA-LDL might be associated with greater lipid and lower fibrous content, contributing to coronary plaque vulnerability. (Circ J 2016; 80: 2173-2182).

Residual risk of cardiovascular events after treatment with stain might be explained in part because patients have low levels of n−3 polyunsaturated fatty acids (PUFA). We examined how lipid-lowering therapy with strong statin affected serum PUFA levels in patients with coronary artery disease. The study population consisted of 46 patients with coronary artery disease whose low-density lipoprotein (LDL) cholesterol was more than 100 mg/dl. Lipid-lowering therapy was performed with a strong statin including atorvastatin (n = 22), rosuvastatin (n = 9) or pitavastatin (n = 15). Serum PUFA levels were determined by gas chromatography. The treatment with strong statin decreased the sum of dihomo-γ-linolenic acid (DGLA) and arachidonic acid (AA) levels (195 ± 41 to 184 ± 44 μg/ml, P < 0.05) as well as the sum of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) levels (233 ± 71 to 200 ± 72 μg/ml, P < 0.001). These effects of strong statin resulted in a significant decrease in ratio of the sum of EPA and DHA levels to the sum of DGLA and AA levels (1.20 ± 0.27 to 1.10 ± 0.35, P < 0.05). The percent decrease in the LDL cholesterol level correlated significantly with that in the sum of EPA and DHA levels (r = 0.38, P < 0.01). In conclusion, our results showed that lipid-lowering therapy with strong statin mainly reduced n−3 PUFAs in proportion to the decrease in the LDL cholesterol level in patients with coronary artery disease.

Aliskiren is a novel blood pressure-lowering agent acting as an oral direct renin inhibitor. We evaluated the effects of aliskiren on the fibrinolytic system in patients with coronary artery disease who were receiving angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II type 1 receptor blockers (ARBs). We studied 17 patients with coronary artery disease whose systolic blood pressure was more than 130 mmHg despite treatment with ACEIs or ARBs. Aliskiren (150 mg) was added to ACEIs or ARBs, and was continued for 6 weeks. Aliskiren significantly decreased systolic blood pressure (140 ± 6-128 ± 8 mmHg, P < 0.001) and plasma renin activity (1.8 ± 2.3-0.6 ± 0.9 ng/ml/h, P < 0.01) after 6 weeks. However, it did not affect plasminogen activator inhibitor-1 (28.8 ± 14.5-30.6 ± 13.6 ng/ml, P = 0.84), fibrinogen (305 ± 72 vs 301 ± 71 mg/dl, P = 0.33), or D-dimer (0.49 ± 0.24-0.51 ± 0.28 μg/ml, P = 0.70) levels. Our data suggested that patients receiving ACEIs or ARBs would not be expected to have any changes in biomarkers of the fibrinolytic system with additional pharmacologic inhibition of the renin-angiotensin-aldosterone system.

Background: Several reports have recently described the variant form of takotsubo cardiomyopathy exhibiting midventricular ballooning. The purpose of this study was to assess electrocardiographic (ECG) findings on admission in patients with midventricular ballooning. Hypothesis: ECG findings are different between the midventricular ballooning form and apical ballooning form of takotsubo cardiomyopathy. Methods: We reviewed ECGs on admission in 6 patients with midventricular ballooning and 20 patients with apical ballooning. The sum of ST segment elevation in leads V1 to V3 or in leads V4 to V6 was obtained. The number of leads showing ST segment elevation and/or T wave inversion was also obtained. These ECG findings were compared between the 2 groups. Results: In midventricular ballooning, ECG changes including ST segment elevation and/or T wave inversion were observed frequently in leads V2 and V3, and were not observed in leads II, III, −aVR, aVF, V5, and V6. On the other hand, in apical ballooning, they were found in all leads. They were most common in leads V4 and V5. The sum of ST segment elevation in leads V1 to V3 was similar (2.6 ± 2.0 mm vs 2.7 ± 2.0 mm, P = not significant), and the sum of ST segment elevation in leads V4 to V6 was significantly lower in midventricular ballooning than apical ballooning (0.4 ± 0.8 mm vs 3.5 ± 3.0 mm, P

Background: The transradial approach has several pitfalls that include problems regarding the radial puncture and difficulties with the catheter technique. We evaluated whether external side-compression of radial artery was helpful to yield the success rate for advancement of guidewires under the presence of side branches or arterial tortuosity. Methods and Results: The study population consisted of 11 patients with unsuccessful advancement of guidewires into the brachial artery. In 7 patients, the J-tip hydrophilic guidewire was not advanced into the brachial artery because it always directed into the side branch. During external side-compression of radial artery at the culprit site with a finger of the second operator, the guidewire was successfully advanced into the brachial artery in all patients. In 4 patients, the guidewire was not advanced into the brachial artery because the radial artery was tortuous. During external side-compression of radial artery at the culprit site, the guidewire was successfully advanced into the brachial artery in 2 patients. In the remaining 2 patients in whom this attempt was unsuccessful, coronary angiography was performed through the right brachial artery. Overall success rate of this technique was 82%. Conclusion: External side-compression of radial artery is an easy and feasible technique for difficulties in the advancement of guidewires due to the presence of side branches or arterial tortuosity. (J Interven Cardiol 2011;24:397–400)

To compare the cardioprotective effect of prodromal angina pectoris and collateral circulation, 245 patients with first anterior acute myocardial infarction who underwent coronary angioplasty within 12 hours of symptoms were studied. Prodromal angina pectoris and collateral circulation were independently associated with higher predischarge left ventricular ejection fraction (LVEF), and a combination of prodromal angina pectoris and collateral circulation afforded cumulative improvement in LVEF in patients without diabetes mellitus. In patients with diabetes mellitus, collateral circulation, but not prodromal angina pectoris, was associated with higher predischarge LVEF.

Background In the percutaneous coronary intervention (PCI) era, the impact of initial ST-segment elevation magnitude on left ventricular (LV) function in patients with acute myocardial infarction (AMI) remains unclear. Methods and Results In the present study, 239 patients with total occlusion and 81 patients with spontaneous reperfusion within 12 h of their first anterior AMI were evaluated. The sum of ST-segment elevation (ΣST) was measured in leads I, aVL and V1-6 shortly before angiography. Predischarge LV ejection fraction (LVEF) was obtained at 15±5 days. In total occlusion, the predischarge LVEF was significantly lower in patients with ΣST ≥10 mm than in those with ΣST

Background The time course of the electrocardiographic (ECG) changes in patients with tako-tsubo syndrome remains unknown. Methods and Results In the present study, 16 patients with tako-tsubo syndrome and 15 patients with anterior acute myocardial infarction with minimal enzymatic release (minimal AMI) were evaluated. Left ventricular dysfunction dramatically resolved approximately 2 weeks later in both groups. In the patients with tako-tsubo syndrome, the admission ECG usually showed ST segment elevation, especially in leads V3-6. T wave inversion deepened progressively to its first negative peak, which occurred at approximately 3 days. The T wave was shallow for several days and then deepened again, the second negative peak occurring at approximately 2-3 weeks. The QT interval was prolonged as the T wave deepened, and shortened as the T wave became shallow. In the patients with minimal AMI, a similar time course of ECG changes was observed after reperfusion. In general, at 3 days or later during the early phase, T wave inversion was deeper and the QTc interval was longer in tako-tsubo syndrome than in minimal AMI. Conclusions Because the time course of the ECG changes, as well as that of the left ventricular dysfunction, is similar between tako-tsubo syndrome and minimal AMI, these 2 cardiac disorders must be carefully differentiated. (Circ J 2004; 68: 77 - 81)

Claudia Borgioni, Roberto, et al. Adverse prognostic significance of new diabetes in treated hypertensive subjects. Hypertension 2004;43:963–9. [5] Rashed Al Bannay, Husain. Aysha. Hypertensive crisis: clinical presentation, comorbidities, and target organ involvement. Saudi Med J 2010;31(8):916–20. [6] Avanzini F, Marchioli R, Alli C, Tognoni G. HypertensionOptimal Treatment (HOT) trial. Lancet 1998;352:571–2. [7] Patel Anushka, MacMahon Stephen, Chalmers John, Neal Bruce, Billot Laurent, Woodward Mark, et al. Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes The ADVANCE Collaborative Group*. N Engl J Med 2008;358:2560–72. [8] Shigeru Nakano, Kazunori Konishi, Keisuke Furuya, Keigo Uehara,Makoto Nishizawa, Atsushi Nakagawa, et al. A prognostic role of mean 24-h pulse pressure level for cardiovascular events in type 2 diabetic subjects under 60 years of age. Diabetes Care 2005;28(no 1):95–100 January. [9] Tomas LG, Andersson, Raymond G, GoslingPhilip J, Chowienczyk, Ronan P, Kelly, Helen MacCallum, Millasseau Sandrine C. Photoplethysmographic assessment of pulse wave reflection blunted response to endothelium-dependent beta2adrenergic vasodilation in type ii diabetes mellitus. J Am Coll Cardiol 1999;34:2007–14. [10] Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin P. Hypertensive urgencies and emergencies, prevalence and clinical presentation. Hypertension 1996;27: 144–7. [11] Martin JF, Higashiama E, Garcia E, Luizon R, Cipullo J. Hypertensive crisis profile: prevalence and clinical presentation. Arq Bras Cardiol 2004;83:125–30. [12] Haffner Steven M. Dyslipidemia management in adults with diabetes. Diabetes Care January 2004;27:s68–71. [13] Emberson Jonathan, Bennett Derrick, Link Emma, Parish Sarah, Danesh John, Armitage Jane, et al. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo controlled trial. Lancet 2002 Jul 6;360(9326):7–22. [14] Andrews. Peter. Renal dysfunction as a marker of increased vascular risk. British Journal of Diabetes & Vascular Disease 2004;4:152. [15] Dzau V, Braunwald E, Participants. Resolved and unresolved issues in the prevention and treatment of coronary artery disease: a workshop consensus statement. Am Heart J 1991;121:1244–62.

Mean platelet volume (MPV) is a well-established marker of platelet activation, and recent studies have shown that platelet activation is central to the processes in the pathophysiology of coronary artery disease (CAD). The study population consisted of 45 patients with stable CAD who underwent successful percutaneous coronary intervention (PCI) with drug-eluting stents. We selected 45 age- and sex-matched control subjects without cardiovascular diseases who did not require antiplatelet therapy. Hematological test was performed 3 times within 1 month before DAPT (baseline), at 2 weeks after PCI (post PCI) and at 9 months after PCI (follow-up). Compared to control subjects, MPV was significantly larger in patients with CAD (10.0 ± 0.6 vs 10.7 ± 0.8 fl, p < 0.01) although there was no significant difference in white blood cell count, hemoglobin, and platelet count between the 2 groups. In patients with CAD, DAPT did not affect platelet count (19.3 ± 4.8 × 104–18.9 ± 4.6 × 104/μl) or MPV (10.7 ± 0.8–10.5 ± 0.9 fl) during the follow-up period. MPV remained to be higher at follow-up in patients with CAD despite DAPT compared to control subjects (10.1 ± 0.7 vs 10.5 ± 0.9 fl, p < 0.05). Our data suggested that MPV might not be suitable for monitoring the effects of DAPT on platelet activity in patients with CAD undergoing PCI.

Residual risk of cardiovascular disease might stem, at least partially, from low serum concentrations of n-3 polyunsaturated fatty acid (PUFA). The purpose of this study was to evaluate the effects of ezetimibe on serum lipids and PU-FAs in patients with coronary artery disease who were intolerant of new or high-dose statin therapy. The study population consisted of 13 patients who were intolerant of new statin therapy and 10 patients who were intolerant of high-dose statin therapy for the treatment of low-density lipoprotein (LDL) cholesterol. Patients who were intolerant of high-dose statin therapy continued taking a statin, but at a lower dose during the study period. Blood samples were collected before and 12 weeks after ezetimibe (10 mg). We measured serum lipids and PUFAs including dihomo-γ-linolenic acid, arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid. Ezetimibe significantly decreased LDL cholesterol (138 ± 19 mg/dL to 97 ± 34 mg/dL, P < 0.01), but did not significantly affect high-density lipoprotein cholesterol, triglyceride, or any of the PUFAs measured during the follow-up period. Consequently, it did not affect the ratio of EPA to AA (0.40 ± 0.17 to 0.43 ± 0.18, P = ns) or the ratio of n-3 PUFA to n-6 PUFA (1.10 ± 0.39 to 1.09 ± 0.36, P = ns) during the follow-up period. Ezetimibe in combination with a low-dose statin, or as monotherapy in statin-intolerant patients, decreased LDL cholesterol, but did not significantly affect serum PUFA concentrations in patients with coronary artery disease.

A segment of coronary arteries traveling through the myocardium is known as myocardial bridging. Several reports have shown reduced fractional flow reserve (FFR) associated with myocardial bridging. We report a case in which FFR was measured in the left anterior descending artery involving both myocardial bridging and fixed stenosis. Learning objective: We demonstrated a case in which fractional flow reserve (FFR) was measured in the left anterior descending artery involving both myocardial bridging and fixed stenosis. Measurement of FFR was useful to guide PCI for the lesion modified by myocardial bridging.>

A 26-year-old man was admitted to our hospital because of acute pericarditis. The current patient had a saddle-back type ST-segment elevation shortly after the onset of acute pericarditis. Interestingly, it converted into a coved type ST-segment elevation, subsequently regressed gradually as acute inflammation improved. After 3 months, right ventricular rapid pacing induced ventricular fibrillation, and intravenous sodium channel blocker induced a coved type ST-segment elevation. The current case implies that a Brugada-type ST-segment elevation, which is thought to be false in acute pericarditis, may be true in some patients with asymptomatic Brugada syndrome.

A-55-year-old man with diabetes mellitus was admitted to hospital because of chest pain. He was diagnosed as anterior acute myocardial infarction and treated with stent placement. After 7 days, ventricular fibrillation occurred because of a subacute reocclusion and balloon angioplasty was performed. Despite reperfusion therapy, intraaortic balloon pumping, antiarrhythmic drugs and beta-blocker, ventricular tachycardia or fibrillation relapsed and cardioversion was performed 29 times during 32 h. Temporary overdrive atrioventricular sequential pacing was initiated and the malignant arrhythmia finally disappeared. Even after stoppage of 25 h overdride pacing, it never recurred. Temporary overdrive pacing is an easy and feasible therapy for a drug-resistant electrical storm associated with AMI and should be performed in the early stage.

Background It remains unclear whether spontaneous anterograde flow preserves myocardial fatty acid metabolism in patients with acute myocardial infarction (AMI). Methods and Results The present study comprised 129 patients with a first anterior AMI in whom Thrombolysis in Myocardial Infarction (TIMI) 3 flow was obtained on the final angiogram: 28 patients with spontaneous anterograde flow and 101 patients with total occlusion on the initial angiogram. Thallium-201 (201Tl) and iodine-123-β-methyl-p-iodophenyl penta-decanoic acid (123I-BMIPP) dual-isotope myocardial single-photon emission computed tomography (SPECT) was performed at 6.5±4.2 days after onset. The SPECT image was divided into 17 segments, and each segment was graded with scores between 0 and 4 (0, normal uptake; 4, defective). The sum of each score was defined as the total defect score (TDS). TDS values for 201Tl (9.0 ±7.4 vs 16.8±12.2, p

AIM: To investigate the effects of different doses of aspirin on coronary endothelial function. METHODS: The study included 139 Japanese subjects (mean age, 60 years; 53 women) with angiographically normal coronary arteries. Patients were distributed into Group Ⅰ (n = 63), who was administered aspirin and Group Ⅱ (n = 76), the control, who were not administered aspirin. Group Ⅰ was further divided into Group Ⅰa (n = 50, low-dose aspirin, 100 mg) and Group Ⅰb (n = 13, high-dose aspirin, 500 mg). After a routine coronary angiography, acetylcholine (ACh; 3 and 30 µg/min successively) and nitroglycerin (NTG) were infused into the left coronary ostium over 2 min. The change in the diameter of the coronary artery in response to each drug was expressed as the percentage change from baseline values. RESULTS: The patient characteristics did not differ between the two groups. The change in coronary diameter in response to ACh was greater in Group Ⅰ than in Group Ⅱ (P = 0.0043), although the NTG-induced coronary vasodilation was similar between groups. ACh-induced dilation was greater in Group Ⅰa than in Group Ⅰb (P = 0.0231). Multivariate regression analysis showed that a low-dose of aspirin (P = 0.0004) was one of the factors associated with ACh-induced dilation at 30 µg/min. CONCLUSION: In subjects with angiographically normal coronary arteries, aspirin only had a positive influ ence on coronary endothelial function at the low dose of 100 mg. This improvement of coronary endothelial function may be involved in the preventive effect of aspirin against future coronary events.

AIM: To investigate endothelium-dependent and -independent coronary microvascular functions in patients with vasospastic angina (VSA). METHODS: Thirty-six patients with VSA (30 men and 6 women; mean age, 58 years) were enrolled in this study. VSA was defined as ≥ 90% narrowing of the epicardial coronary arteries on angiography performed during a spasm provocation test, presence of chest pain, and/or ST-segment deviation on an electrocardiogram (ECG). Patients (n = 36) with negative spasm provocation test results and those matched for age and sex were enrolled as a control group (nonVSA group). Low-dose acetylcholine (ACh; 3 μg/min) was infused into the left coronary ostium for 2 min during the spasm provocation test. Following the spasm provocation test, nitroglycerin (0.2 mg) was administered intracoronally. Coronary blood flow (was calculated from quantitative angiography and Doppler flow velocity measurements, and the coronary flow reserve was calculated as the ratio of coronary flow velocity after injection of adenosine triphosphate (20 μg) to the baseline value. Changes in the coronary artery diameter in response to ACh and nitroglycerin infusion were expressed as percentage changes from baseline measurements. RESULTS: Body mass index was significantly lower in the VSA group than in the nonVSA group. The frequency of conventional coronary risk factors and the rate of statin use were similar between the 2 groups. The left ventricular ejection fraction as evaluated by echocardiography was similar between the 2 groups. The duration of angina was 9 ± 2 mo. The results of blood chemistry analysis were similar between the 2 groups. Low-dose ACh did not cause coronary spasms. The change in coronary artery diameter in response to ACh was lower in the VSA group (-1.4% ± 9.3%) than in the nonVSA group (3.1% ± 6.5%, P < 0.05), whereas nitroglycerin-induced coronary artery dilatation and coronary blood flow increase in response to ACh or coronary flow reserve did not differ significantly between the 2 groups. CONCLUSION: These findings suggest that microvascular coronary function may be preserved despite endothelial dysfunction of the epicardial coronary arteries in patients with VSA.

To assess coronary endothelial function of conduit and resistance vessels in patients with metabolic syndrome (MS).Seventy-eight men (mean age, 57 years) with chest pain and angiographically normal coronary arteries were included in the study. Patients with coronary spastic angina were excluded. Changes in coronary artery diameter and coronary blood flow (CBF) in response to acetylcholine (ACh) were determined using quantitative coronary angiography and Doppler velocity measurements. Coronary flow reserve was calculated as the ratio of coronary blood velocity after adenosine triphosphate infusion relative to baseline values. Patients were divided into two groups based on the presence or absence of MS.There were 24 patients in the MS group (31%). The increase in CBF in response to ACh infusion was impaired in the MS group (P0.0001) compared to the non-MS group, whereas changes in coronary artery diameter in response to ACh infusion did not differ between the two groups. Multivariate regression analysis revealed that MS was a significant factor associated with the lesser change in CBF induced by ACh infusion at 30 μg/min (P0.0001, r(2) = 0.46).Coronary endothelial dysfunction was present at the level of resistance vessels but not conduit vessels in the MS patients included in our study.