Biomedical subjects

S Morooka

Publications and source records attributed to S Morooka.

At least 73 records · Page 4Linked to original sources

PubMed1996

Reduction of rat myocardial ischemia and reperfusion injury by sialyl Lewis x oligosaccharide and anti-rat P-selectin antibodies.

Polymorphonuclear leukocytes (PMN) are directly involved in development of ischemic myocardial injury. Adhesion of PMN to endothelial cells is an initial step that triggers a sequential process leading to acute inflammatory responses. Interaction between P-selectin and its oligosaccharide ligand, sialyl Lewis x (sLex), plays an important role in the early stage of the adhesion. To examine the role of P-selectin in various animal disease models especially in rats, we have cloned rat E- and P-selectin cDNAs and established monoclonal antibodies against these rat selectins. In this report, we describe the generation and characterization of anti-rat P-selectin antibodies (ARPs). These antibodies detect cell surface P-selectin on thrombin-stimulated rat platelets. More importantly, intravenous administration of ARP2-4 reduced infarction developed after 30 min of ischemia followed by 24 h of reperfusion in a rat myocardial injury model. In addition, similar protective effect was also observed by administration of a sLex-oligosaccharide. These results indicate that cell adhesion mediated via P-selectin is involved in the development of ischemia and reperfusion injury in rat heart.

Animals↗

PubMed1996

Early detection of platelet activation after coronary angioplasty.

BACKGROUND: Although platelet activation has been considered an important reaction after percutaneous transluminal coronary angioplasty (PTCA), it is still difficult to detect the activated platelets in vivo directly. METHODS: To detect platelets activated at an early stage after PTCA, blood samples were take from the coronary sinus and the aorta in 22 patients with coronary artery disease, who underwent PTCA for a lesion of the left anterior descending artery. Ten patients with coronary artery disease, who underwent diagnostic coronary angiography only, were compared with them. The expression of activation-dependent granular protein, CD62P (P-selectin) and CD63, on the platelet membrane surface was analysed using flow cytometry. The plasma thrombomodulin level was also measured. RESULTS: The percentage of platelets positive for CD62P (0.53 +/- 0.04 to 0.80 +/- 0.11%, P < 0.01) and CD63 (16.0 +/- 1.4 to 19.8 +/- 2.0%, P < 0.05) increased after PTCA in the coronary sinus, although it did not change in the aorta. The plasma thrombomodulin level also increased after PTCA in the coronary sinus (16.7 +/- 1.0 to 20.4 +/- 2.0 mu/ml, P < 0.05). However, these parameters did not change after coronary angiography only. After PTCA, the plasma thrombomodulin level was correlated with the percentage of platelets positive for CD62P (r = 0.88, P < 0.001) and with that for CD63 (r = 0.69, P < 0.001) in the coronary sinus. CONCLUSIONS: PTCA produced activation of circulatory platelets, which might have been caused by balloon-induced vascular endothelial injury. One should take care to avoid needless vascular injury during the PTCA procedure to inhibit the platelet activation.

Angioplasty, Balloon, Coronary↗

PubMed1996

Relationship of thallium-201 clearance on exercise stress myocardial scintigraphy to coronary flow reserve in patients with coronary artery disease.

OBJECTIVE: We evaluated thallium-201 (201Th) clearance measurement during exercise myocardial scintigraphy in patients with coronary artery disease, for the assessment of coronary circulatory function and diagnosis. DESIGN: The clearance rate of 201Th was compared with the coronary flow reserve measured by Doppler coronary flow velocimetry. METHODS: We selected 20 patients who had chronic stable angina with single-vessel coronary artery disease of the left anterior descending artery (LAD) and underwent percutaneous transluminal coronary angioplasty (PTCA). Ten control patients had atypical chest pain but no detectable heart disease. Regional net clearance of 201Th was measured from the early and delayed bull's-eye images of 201Th exercise stress single photon emission tomography (SPECT). Using a Doppler catheter, we also measured coronary flow reserve of the LAD, which was obtained by the intracoronary administration of papaverine. RESULTS: The net 201Th clearance in the anterior wall myocardium in the patients with coronary artery disease before PTCA was significantly less than that in the controls. At follow-up angiography after successful PTCA, it increased. The coronary flow reserve before PTCA was also lower than that in the controls. It was increased immediately after PTCA, and was more markedly increased at the follow-up angiography. Before PTCA, regional net clearance in the anterior myocardium was correlated with the coronary flow reserve of the LAD. The ratio for the net clearance of the anterior myocardium at follow-up angiography to that before PTCA was also correlated with the ratio for coronary flow reserve. CONCLUSIONS: In patients with coronary artery disease, the regional 201Th clearance in the ischaemic area measured by exercise 201Th SPECT is correlated with the coronary flow reserve of the affected artery. Moreover, the increase in the clearance rate after PTCA is also correlated with that in the coronary flow reserve. Thus the measurement of regional 201Th clearance might be a useful non-invasive method of estimating of the coronary flow reserve.

Analysis of Variance↗

PubMed1996

An effective tool to detect lesions causing unstable angina with multivessel disease: iodine-123-betamethyl-p-iodophenyl-pentadecanoic acid single photon emission computed tomography.

Radiolabeled fatty acids such as iodine-123-betamethyl-p-iodophenyl-pentadecanoic acid (BMIPP) have unique metabolic properties suggesting potential use as myocardial perfusion tracers. The uptakes of BMIPP and thallium 201 were compared using single photon emission computed tomography (SPECT) in 24 patients displaying unstable angina with multivessel disease at a mean of 3.4 days after admission. Coronary angiography was performed within a week. Uptake was considered normal if the activity was greater than 80% of the normal area, mildly reduced if 50% to 79%, and severely reduced if less than 50%. The regional activities in four quardrants in short-axis slices were measured from basal, mid and apical sets. We attempted to identify the causative lesion on dual SPECT imaging. We planned the following management of each patient based on the results of the dual SPECT study. BMIPP activity imaging found 4 segments (1.4%) with severe decrease, 70 (24.3%) with mild decrease, and 214 (74.3%) with normal uptake. In contrast, T1 activity imaging showed normal uptake in 68 of 74 abnormal BMIPP activity segments. Furthermore, all segments with abnormal BMIPP uptake were matched with locations of coronary artery stenosis by coronary angiography. Accordingly, coronary revascularization (percutaneous transluminal coronary angioplasty, coronary artery bypass grafting) was performed based on BMIPP SPECT. Reductions in BMIPP activity were common in patients with unstable angina with multivessel disease. BMIPP SPECT is an excellent tool for detecting the causative lesion in unstable angina. The subsequent intervention could be performed with less risk based on the strategy of dilating the only causative lesion which was detected by the BMIPP SPECT in patients with multivessel disease displaying unstable angina.

Angina, Unstable↗

PubMed1996

Safety and effectiveness of exercise training in patients with silent myocardial ischemia.

The effectiveness of exercise training in patients with silent myocardial ischemia was examined. Forty patients with coronary heart disease (mean age 55 +/- 8 years) were recruited for a 12-week exercise training program. All patients underwent treadmill exercise stress testing, exercise thallium-201 single photon emission computed tomography and left heart catheterization. They were divided into three groups based on the symptoms and the results of exercise thallium scintigraphy, i.e., painful myocardial ischemia (PMI group), silent myocardial ischemia (SMI group), and non-myocardial ischemia (NMI group). Normalized treadmill time was longer in the SMI group (108 +/- 24%) than in the PMI group (86 +/- 14%, p < 0.05). All 40 patients, 14 from the PMI group, 16 from the SMI group and 10 from the NMI group, completed the whole exercise training program. A significant prolongation of treadmill time was attained in all three groups after exercise training [PMI group: from 494 +/- 105 to 632 +/- 78 sec (p < 0.05), SMI group: from 609 +/- 147 to 746 +/- 137 sec (p < 0.05), NMI group: from 572 +/- 112 to 739 +/- 13 sec (p < 0.05)]. The improvement of myocardial ischemia following exercise training was similar in the SMI and PMI groups. No adverse effects were detected throughout the program. The exercise training program adopted in this study proved safe and effective in patients with silent myocardial ischemia.

Adult↗

PubMed1995

Lipoteichoic acid-induced neutrophil adhesion via E-selectin to human umbilical vein endothelial cells (HUVECs).

We investigated whether lipoteichoic acid (LTA) induces the expression of E-selectin and neutrophil adhesion to human umbilical vein endothelial cells (HUVECs). LTA (0.01-30 micrograms/ml) induced the expression of E-selectin in a concentration-dependent manner with maximal response at 10 micrograms/ml. The expression level of E-selectin increased from 2 h after stimulation by LTA with the maximal level at 4-8 h. Neutrophil adhesion to LTA-treated HUVECs correlated with the levels of E-selectin expression. In addition, the adhesion was clearly inhibited by anti-human E-selectin monoclonal antibody CY-1787 as well as a sialyl Lewis X (SLeX) oligosaccharide. LTA-induced expression of E-selectin was inhibited by protein kinase C inhibitors, H-7 and staurosporine. These results indicate that LTA induced the expression of E-selectin and neutrophils adhered to HUVECs via E-selectin.

Cell Adhesion↗

PubMed1995

Sialyl Lewis X moiety on rat polymorphonuclear leukocytes responsible for binding to rat E-selectin.

We investigated the presence of the carbohydrate ligand for E-selectin on the cell surface of rat polymorphonuclear leukocytes (PMN). Rat PMN, isolated from peripheral blood, adhered to recombinant rat E-selectin-coated microplates. The adhesion was inhibited either by an anti-rat E-selectin monoclonal antibody (MAb), a sialyl Lewis X (SLex) oligosaccharide or neuraminidase digestion. FACS analysis revealed the expression of SLex as well as other adhesion molecules such as L-selectin, CD11a, CD11b and CD18 on the cell surface of rat PMN. The binding of an anti-SLex MAb KM93 to rat PMN was inhibited competitively by a SLex but not by a Lewis X (Lex). The reactivities of two anti-SLex MAbs, KM93 and CSLEX-1, or an anti-Lex MAb BC90/45 to rat PMN differed from those to human PMN. These results suggest that rat PMN contain the SLex-moiety, which binds to rat E-selectin and is different from that of human PMN.

Animals↗

PubMed1995

Plasma thrombomodulin levels in coronary sinus blood in patients with coronary artery disease.

Plasma thrombomodulin (TM) levels in coronary sinus blood were measured in 15 patients with coronary artery disease who underwent elective PTCA (group A). TM was also measured in eight patients with coronary artery disease (group B) and six patients without coronary artery disease (group C), who only underwent diagnostic coronary angiography. The baseline level was 21.6 +/- 3.4 U/ml in group A, and 21.0 +/- 4.9 in group B, and both levels were slightly higher (P < 0.05) than those in group C (15.1 +/- 3.3). In group A, the level increased to 27.5 +/- 8.3 (P < 0.01) immediately after PTCA and then returned to 22.2 +/- 5.1 by 24 h. In groups B and C, levels showed no change immediately after angiography. In group A, the percentage increase in the TM level immediately after PTCA from that before the procedure correlated with the number of balloon inflations (r = 0.76, P < 0.01). In conclusion, the plasma TM level in coronary sinus blood might indicate endothelial damage due to atherosclerotic coronary artery disease and an increase in the level after PTCA might directly indicate vascular injury by balloon inflation.

Aged↗

PubMed1995

Heart failure progression due to secondary organ dysfunction in acute heart failure.

Although the pathophysiology of heart failure progression is important to survival it is not fully understood. In 92 patients with acute heart failure due to myocardial infarction or dilated cardiomyopathy, secondary organ dysfunction was evaluated to determine whether this factor contributed to heart failure progression and death. Forty-one patients had renal dysfunction, hepatic disease or loss of consciousness after the onset of the acute heart failure, and 26 of them (63%) died of progressive heart failure during the follow-up period of 20 months on average. The one-year survival rate was 22%. Although 51 other patients showed the same initial clinical features and cardiac function, they did not develop concurrent organ dysfunction during the course and only 11 (22%, p < 0.001) died of progressive heart failure. The one-year survival rate was 67%. The survival rate decreased in the order of renal dysfunction, hepatic disease and loss of consciousness. Transient low cardiac output of less than 2.2 l/min/m2 was more frequent in patients with organ dysfunction. It is suggested that heart failure progresses, in part, due to organ dysfunction secondary to heart failure and careful treatment to prevent organ dysfunction is important to long term survival.

Acute Disease↗

PubMed1995

Systemic amyloidosis following ankylosing spondylitis associated with congestive heart failure. A case report.

We report the case of a 38-year-old man who developed fatal, systemic amyloidosis following ankylosing spondylitis. He was admitted for symptoms of congestive heart failure. Based on parotid gland biopsy and echocardiography, he was diagnosed as having systemic amyloidosis following active ankylosing spondylitis. However, the clinical course was rapidly progressive and eventually the patient died of acute necrotizing pancreatitis. The association has been reported thus far in a limited number of cases worldwide. The literature has featured localized lesions and a benign clinical course of the amyloidosis. This case, the first report from Japan, indicates that the amyloidosis associated with ankylosing spondylitis might exhibit a rapidly progressive clinical course, thereby suggesting that in such a case, meticulous treatment is required.

Acute Disease↗

PubMed1994

Effects of platelet activating factor receptor antagonists on intracellular platelet activating factor function in neutrophils.

We investigated the effects of the platelet activating factor (PAF) receptor antagonists, SM-12502 ((+)-cis-3,5-dimethyl-2-(pyridyl)- thiazolidin-4-one hydrochloride), WEB-2086 (3-(4-(2-chlorphenyl)-9-methyl-6H-thieno(3,2-f)-(1,2,4)triazolo(4, 3- a)(1,4)diazepin-2-yl)-1-(4-morpholinyl)-1-propanone) and RP-48740 (3-(3-pyridyl)-1H,3H-pyrrolo[1,2-c]thiazole-7-carboxamide) on the PAF-mediated activation of rat neutrophils. These antagonists inhibited PAF-induced degranulation and chemotaxis in neutrophils at a dose that correlated well with PAF-induced platelet aggregation based on the statistical analyses. N-formyl-L-methionyl-L-leucyl-L- phenylalanin (fMLP)-induced cellular responses were also inhibited by the PAF receptor antagonists, but their inhibitory potencies did not correlate with those for PAF-induced platelet aggregation. In addition, the doses required for inhibition were higher than those required against PAF-induced responses (i.e. IC50 ratio of WEB-2086, SM-12502 and RP-48740 in fMLP-induced/PAF-induced degranulation was 40.0, 2.8 and 5.6, respectively). PAF receptor antagonists inhibited inositol 1,4,5-triphosphate production and the release of Ca2+ from the intracellular store site after stimulation with PAF. In the fMLP-induced responses, PAF receptor antagonists did not inhibit IP3 production and Ca2+ release, but did inhibit transmembrane Ca2+ influx. These results suggest the presence of distinct PAF receptor subtype, to which exogenously added PAF binds, while endogenously produced PAF binds to the other. Intracellular PAF, which was produced by fMLP-stimulation, may play an important role in the late phase of signal transduction, and may participate in the transmembrane Ca2+ influx.

Animals↗

PubMed1994

Vasodilatory capacity of coronary resistance vessels in dilated cardiomyopathy.

Both the endothelium-dependent and endothelium-independent vasodilatory responses of coronary resistance vessels were studied in patients with dilated cardiomyopathy (DCM). A 3F coronary Doppler catheter was placed in the proximal left anterior descending artery in 14 patients with DCM and in 10 patients with chest pain syndrome and a normal heart (control subjects). The ratio of maximum mean coronary blood flow velocity after intracoronary administration of the endothelium-independent vasodilator papaverine (10 mg) to resting mean coronary blood flow velocity (Vp/Vo) in patients with DCM was diminished compared with that in control subjects (2.2 +/- 0.6 vs 4.1 +/- 0.9, p < 0.001). The ratio after administration of the endothelium-dependent vasodilator acetylcholine (40 micrograms) (Va/Vo) in 10 DCM patients was also diminished compared with that in seven control subjects (1.3 +/- 0.5 vs 2.4 +/- 0.8, p < 0.01). In DCM patients, Vp/Vo was correlated with left ventricular end-diastolic pressure (r = -0.48, p < 0.05), left ventricular end-diastolic volume index (r = -0.68, p < 0.01), ejection fraction (r = 0.75, p < 0.01), and left ventricular end-diastolic wall stress (r = -0.73, p < 0.01). However, Va/Vo was not correlated with any of these parameters. These results indicate that impairment of the vasodilatory capacity of coronary resistance vessels in DCM may be related to endothelial dysfunction and to an extravascular factor resulting from left ventricular dysfunction.

Acetylcholine↗

PubMed1994

QT prolongation and possibility of ventricular arrhythmias after intracoronary papaverine.

The incidence of ventricular arrhythmias following the intracoronary injection of papaverine was assessed. A 3F coronary Doppler catheter was placed in the proximal left anterior descending artery and 6-12 mg of papaverine was injected into the left coronary artery in 42 patients. After intracoronary papaverine, the corrected QT interval on the electrocardiogram was prolonged from 0.43 +/- 0.03 to 0.49 +/- 0.07 s (p < 0.001). Occasional premature beats were observed in 2 patients (4.5%) with dilated cardiomyopathy. In 1 patient (2.3%) with 99% stenosis of the left anterior descending artery, polymorphous ventricular tachycardia with marked QT prolongation occurred. This patient also had hypokalemia (2.5 mEq/l) due to primary aldosteronism. In conclusion, careful use of intracoronary papaverine is necessary because of the risk of occasional serious ventricular arrhythmias.

Adult↗

PubMed1994

Days required for 75% suppression of ventricular premature contractions by antiarrhythmic agents obtained from continuous in-hospital ECG monitoring.

To determine the number of days required to obtain 75% suppression of ventricular premature contractions (VPCs) by antiarrhythmic agents, which was expressed as t1/4, we performed 32 in-hospital continuous all day ECG monitoring trials in four groups of 28 symptomatic patients (ages; 54 +/- 20 years-old) with frequent VPCs. Nine patients had no organic heart disease (group 1, 11 trials), nine had valvular heart disease (group 2, 10 trials), three had dilated cardiomyopathy (group 3, 3 trials) and seven had myocardial infarction within two to four weeks onset (group 4, 8 trials). All patients were monitored by ECG telemetry with an arrhythmia analyzer, which could count hourly and daily VPCs. Class I antiarrhythmic agents were given in 18 trials, class II in two trials and class I+ class II in 12 trials. Plasma concentrations of the antiarrhythmic agents were monitored in 11 trials. In 21 trials, t1/4 could be obtained; ten (91%), six (60%), three (100%) and two trials (25%) in the four groups, respectively (p < 0.05). The value of t1/4 in the four groups was 6 +/- 6, 7 +/- 6, 14 +/- 11 and 13 +/- 2 days, respectively (mean 8 +/- 7 days; N.S.). Immediate response to the initial antiarrhythmic agent administration, expressed as percent VPC count after three hours, correlated significantly with t1/4 (r = 0.696, p = 0.0006), but ejection fraction, patient's age, control VPC counts or plasma antiarrhythmic agent level did not correlate with t1/4. In conclusion, t1/4 is a useful index for the evaluation of VPC suppression, revealing wide inter-individual variations and can be roughly estimated from the immediate response to the initial antiarrhythmic agent administration.

Adolescent↗

PubMed1994

Torsades de pointes in paced patients with sick sinus syndrome after disopyramide administration.

Three ventricular inhibited mode (VVI) pacemaker implanted patients, all above 65 years, female and having sick sinus syndrome suffered from torsades de pointes; one patient after 2.5 years and the other two patients within a day of disopyramide therapy. All had hypopotassemia and plasma disopyramide was below the therapeutic range in two patients. Torsades de pointes was induced following ventricular paced beats and suppressed by cessation of disopyramide in all or by setting a higher pacing rate in one. In our department, permanent VVI pacemakers were implanted in 43 patients with sick sinus syndrome including 26 with bradycardia-tachycardia syndrome, nine of whom were treated by disopyramide. Torsades de pointes was observed only in those disopyramide treated bradycardia-tachycardia patients. Our report stresses the proarrhythmic nature of combined VVI pacing and antiarrhythmic agents in the presence of hypopotassemia.

Aged↗

PubMed1994

Effect of the platelet activating factor antagonist (+)-cis-3,5-dimethyl-2-(3-pyridyl)thiazolidin-4-one hydrochloride on endotoxin-induced hypotension and hematological parameters in rats.

The intravenous administration of endotoxin to anesthetized rats resulted in different hypotensive reactions depending on its dosage. More than 10 mg/kg of endotoxin induced biphasic hypotension; the first phase consisted in a small and transient depression (approximately 15 mmHg) of mean arterial pressure occurred within 1 min after the administration, and the second phase was a large and sustained depression (maximally 40 mmHg) observed from 1 h after the injection. At less than 3 mg/kg of endotoxin, the first phase of hypotension did not occur whereas the second phase of hypotension was observed. Pre-treatment or post-treatment with a specific platelet activating factor (PAF) antagonist, SM-12502 ((+)-cis-3,5-dimethyl-2-(3-pyridyl)thiazolidin-4-one HCl, CAS 119383-00-5) inhibited the second phase of endotoxin (1 mg/kg)-induced hypotension. In addition, post-treatment with another PAF antagonist, (3-(4-(2-chlorophenyl)-9-methyl-6H-thieno (3,2-f) (1, 2,4)-thiazolo-phenone) also inhibited the second phase of hypotension. Blood PAF-like substance level, measured by the PAF radioimmunoassay, slightly increased at 1 min after administration of endotoxin (30 mg/kg). At 90 min after the injection, endotoxin (1 mg/kg) induced a significant increase of PAF-like substance level.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Biological effects of the new platelet-activating factor receptor antagonist (+)-cis-3,5-dimethyl-2-(3-pyridyl)thiazolidin-4-one hydrochloride.

SM-12502 ((+)-cis-3,5-dimethyl-2-(3-pyridyl)thiazolidin-4-one HCl, CAS 119383-00-5) inhibited platelet-activating factor (PAF)-induced aggregation of rabbit and human platelets with IC50 values of 2.3 mumol/l and 4.7 mumol/l, respectively, but did not inhibit platelet aggregation induced by adenosine diphosphate, collagen, thrombin, arachidonic acid, U46619 (a thromboxane A2 agonist) or Ca2+ ionophore A23187 at concentrations up to 400 mumol/l. SM-12502 competitively antagonized 3H-PAF binding to rabbit platelets with an IC50 of 1.0 mumol/l. In contrast, the anti-PAF activity of the optical isomer SM-12501 ((-)-cis-3,5-dimethyl-2-(3-pyridyl)thiazolidin-4-one HCl) was much weaker and its IC50 was more than 100 mumol/l. SM-12502 prevented PAF-induced death in mice with ID50 values of 4.8 mg/kg (i.v.) or 68.6 mg/kg (p.o.). In guinea pigs, SM-12502 inhibited PAF (0.1 micrograms/kg)-induced hemoconcentration with ID50 values of 1.9 mg/kg (i.v.) or 40.2 mg/kg (p.o.). In addition, SM-12502 inhibited PAF (10 ng/kg)-induced hypotension in rats with ID50 values of 2.0 mg/kg (i.v.) or 6.5 mg/kg (p.o.). The in vivo effects of SM-12501 were much weaker. Orally administered SM-12502 showed rapid absorption and a long duration of pharmacological activity in rats. SM-12502 afforded dose-dependent protection against anaphylactic death in mice with ID50 values of 18.4 mg/kg (i.v.) and 136 mg/kg (p.o.). It also inhibited endotoxin (E. coli 0.55:B5, 60 mg/kg)-induced death in mice, with ID50 values of 119 mg/kg (i.v.) and 182 mg/kg (p.o.).(ABSTRACT TRUNCATED AT 250 WORDS)

Anaphylaxis↗

PubMed1993

Coronary flow reserve in patients with dilated cardiomyopathy.

Coronary flow reserve was studied in patients with dilated cardiomyopathy. A 3F coronary Doppler catheter was placed in the proximal left anterior descending artery in each of 10 patients with dilated cardiomyopathy (CDM group), seven patients with coronary artery disease that involved only the left anterior descending artery (CAD group), and seven patients with chest pain syndrome and normal hearts (control group). Coronary flow reserve was calculated as the ratio of the maximum mean coronary blood flow velocity after intracoronary administration of papaverine (10 mg) to resting flow velocity (M/R). The time until maximum flow velocity was reached after papaverine administration (Tmax) was also measured. M/R was lower in the DCM (p < 0.001) and CAD (p < 0.001) groups when compared with the control group. Tmax was not abnormal in the DCM group but was prolonged in the CAD group (p < 0.05). In the DCM group, the M/R ratio correlated with the left ventricular end-diastolic pressure (r = -0.69; p < 0.05), the left ventricular end-diastolic volume index (r = -0.7; p < 0.05), the ejection fraction (r = 0.82; p < 0.01), the left ventricular mass (r = -0.7; p < 0.05), and the left ventricular end-diastolic wall stress (r = -0.84; p < 0.001). These results indicate that coronary flow reserve was decreased in patients with dilated cardiomyopathy and that the mechanism of its reduction may differ from that in patients with coronary artery disease.

Adult↗