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Biomedical subjects

T Crake

Publications and source records attributed to T Crake.

At least 37 records · Page 2Linked to original sources
PubMed1997

Basal and flow-mediated nitric oxide production by atheromatous coronary arteries.

OBJECTIVES: This study assessed the effects of inhibition of nitric oxide synthesis on epicardial human coronary arteries and on coronary flow velocity during baseline conditions and during atrial pacing. BACKGROUND: Epicardial coronary artery dilation occurs in response to an increase in heart rate. It is not known whether the dilation of both angiographically normal and diseased epicardial coronary arteries during atrial pacing is nitric oxide dependent in humans. METHODS: The effects of an intracoronary infusion (4 mumol/min for 8 min) of NG-monomethyl-L-arginine (LNMMA), an inhibitor of nitric oxide synthesis, was studied in 16 patients with coronary artery disease and in 6 patients with normal coronary arteriograms. In all patients atrial pacing was performed during normal saline and during LNMMA infusion. the lumen diameter of epicardial coronary arteries was assessed by quantitative angiography, and changes in blood flow velocity were measured with a Doppler catheter. RESULTS: During saline infusion a significant increase in the lumen diameter of the proximal (p < 0.05) and distal (p < 0.01) segments of both normal and diseased arteries occurred during atrial pacing. No significant lumen diameter changes occurred in either group when atrial pacing was performed during LNMMA infusion. Stenosis diameter decreased during LNMMA infusion but did not change with atrial pacing either during saline infusion or during LNMMA infusion. The mean percent change in coronary blood flow with atrial pacing was less (p < 0.05) during LNMMA infusion than during saline infusion in both groups. CONCLUSIONS: These findings confirm that epicardial coronary artery dilation induced by pacing is nitric oxide dependent. Nitric oxide production contributes to the vasomotor tone of coronary resistance vessels. Nitric oxide is produced at the site of atheromatous stenosis but is unaffected by pacing.

Blood Flow Velocity↗
PubMed1997

Effects of inhibition of nitric oxide synthesis in patients with coronary artery disease and stable angina.

AIMS: Inhibition of nitric oxide synthesis causes a decrease in the basal diameter of normal distal epicardial coronary arteries in normal subjects. The effects of inhibition of nitric oxide in atheromatous coronary arteries is unknown. This study assessed the effects of the inhibition of nitric oxide synthesis in epicardial coronary arteries in patients with coronary artery disease. METHODS AND RESULTS: The effects of an intracoronary infusion of NG-monomethyl-L-arginine (LNMMA, an inhibitor of nitric oxide synthesis), were studied in 13 patients with chronic stable angina and coronary artery disease. The diameter of angiographically normal proximal and distal segments and coronary stenoses was measured by quantitative angiography. In response to an LNMMA infusion of 16 mumol min-1 for 4 min there was a significant reduction (P < 0.01) in the luminal diameter of the distal segments of diseased arteries (from 1.32 +/- 0.07 to 1.17 +/- 0.06 mm) and at the site of stenosis (from 1.15 +/- 0.22 to 1.06 +/- 0.20 mm), but no change (P = NS) in the luminal diameter of the proximal segments (from 3.16 +/- 0.12 to 3.08 +/- 0.14 mm) of diseased arteries. CONCLUSIONS: The average effect of inhibition of basal nitric oxide synthesis in epicardial coronary arteries in patients with stable angina and coronary artery disease was only distal constriction. Coronary stenoses constricted at the highest LNMMA concentration.

Angina Pectoris↗
PubMed1997

Impairment of the myocardial vasomotor response to cold pressor stress in collateral dependent myocardium.

OBJECTIVE: To study the vasomotor response (cold pressor/basal flow) in myocardium perfused entirely by collaterals, using the reflex sympathetic stimulation of cold pressor stress. DESIGN: Regional myocardial blood flow was measured in collateral dependent and in remote myocardium using positron emission tomography with 15O water at basal and at cold pressor stress. Regional ischaemia was measured with 18F-fluorodeoxyglucose (FDG). PATIENTS: Nine patients (mean (SD) age 53 (6) years) with an occluded coronary artery supplied entirely by collaterals from other angiographically normal arteries. RESULTS: In remote myocardium, basal and cold pressor flow were 0.99 (0.26) and 1.46 (0.60) ml/min/g (P < 0.05), respectively, a myocardial vasomotor response of 1.46 (0.45). In collateral dependent myocardium, basal and cold pressor flow were 0.91 (0.20) and 0.87 (0.35) ml/min/g, respectively (the latter value, P < 0.05 v remote region), a myocardial vasomotor response of 0.97 (0.43) (P < 0.05 v remote region). The myocardial vascular resistance (mean arterial pressure/flow) during cold pressor was higher in the collateral dependent than in remote myocardium, at 147.0 (61.1) and 85.6 (32.3) mm Hg.min.g/ml (P < 0.05), respectively, but with no relative increase in FDG uptake. CONCLUSIONS: In contrast to the decrease in myocardial resistance in remote myocardium with cold pressor, an increase was observed in collateral dependent myocardium suggesting a vasoconstrictor response in resistive vessels, without demonstrable myocardial ischaemia.

Cold Temperature↗
PubMed1996

Regional changes in angiotensin II receptor density after experimental myocardial infarction.

The plasma and cardiac renin-angiotensin systems may be activated after myocardial infarction. The myocardium may therefore be exposed to increased concentrations of angiotension II, which may contribute to myocardial injury. The purpose of this study was to identify the potential sites of action of angiotensin II in the infarcted heart. Myocardial infarction was induced in rats by left coronary artery ligation, and the hearts were removed for study after 18 h, 7 days, or 8 months. The regional ventricular angiotensin II receptor density was assessed by [125I](Sar1,Ile8)angiotensin II binding and quantitative autoradiography. The [125I](Sar1,Ile8)angiotensin II binding was unchanged at 18 h, but was increased at 7 days in the infarcted region of the left ventricle (73.2 +/- 3.2 amol/mm2, mean +/- S.E.M.) compared with the non-infarcted region (1.6 +/- 0.2 amol/mm2, P < 0.0001) and with the left ventricular myocardium of sham-operated control animals (1.3 +/- 0.1 amol/mm2, P < 0.0001). The increased [125I](Sar1,Ile8)angiotensin II binding density was still present, but diminished, at 8 months after coronary ligation (49.0 +/- 5.7 amol/mm2, P < 0.0001 v control, P = 0.0058 v 7-day infarcts). The increased binding of [125I](Sar1,Ile8)angiotensin II was antagonised by losartan, an AT1 receptor antagonist, but not by an AT2 receptor antagonist. Microautoradiography of [125I](Sar1,Ile8) angiotensin II, and assessment of collagen deposition using picrosirius staining and immunostaining demonstrated that the regional increase in AT1 receptor density in the infarcted region of myocardium was associated with fibroblast infiltration and collagen deposition. The infarct scar and the cardiac fibroblasts within it express high levels of angiotension II receptors and therefore represent potential targets for the actions of angiotensin II after myocardial infarction.

Animals↗
PubMed1996

Altered resistive vessel function after coronary angioplasty is not due to reduced production of nitric oxide.

BACKGROUND: The coronary vasodilator reserve with dipyridamole may be impaired immediately after successful angioplasty due to reduced endothelial production or release of nitric oxide. As the vasodilator response to exogenous nitrates is enhanced by endothelium removal or inhibition of nitric oxide synthesis, an increased vasodilator response to nitrovasodilators, such as nitroprusside, should occur. METHODS: The coronary vasodilator reserve (maximal/basel coronary blood flow) with intravenous dipyridamole (0.56 mg/min for 4 min) was measured by Doppler catheterization before and after angioplasty in 10 patients with single-vessel coronary disease. At peak dipyridamole effect, incremental doses of nitroprusside (4-50 micrograms/min) were given intracoronary until systolic blood pressure fell by > or = 5 mmHg. RESULTS: Before angioplasty, the coronary blood flow increased from 19.7 +/- 6.1 (mean +/- s.d.) at basal to 30.1 +/- 11.9 ml/min at the peak dipyridamole effect (P < 0.01), giving a coronary vasodilator reserve of 1.62 +/- 0.39 (range 1.20 - 1.96). After angioplasty, the coronary blood flow increased from 32.4 +/- 13.2 at basal to 53.4 +/- 23.3 ml/min at the peak dipyridamole effect (P < 0.01), giving a coronary vasodilator reserve of 1.77 +/- 0.64 (range 1.7-2.42). Sodium nitroprusside had no additional effect on coronary flow (49.5 +/- 20.4 and 52.2 +/- 18.0 ml/min) before and after a fall in systolic blood pressure, respectively. CONCLUSIONS: The vasodilator response to dipyridamole was markedly impaired immediately after successful angioplasty, and was not augmented by intracoronary nitroprusside. Thus, a reduced production or release of nitric oxide in the coronary circulation does not seem to be responsible for the impaired vasodilator response after angioplasty.

Adult↗
PubMed1996

Variable coronary vasomotor responses to acetylcholine in patients with normal coronary arteriograms: evidence for localised endothelial dysfunction.

OBJECTIVE: The vasomotor responses of the epicardial coronary arteries to acetylcholine were examined in patients with normal coronary arteries and chest pain. DESIGN: Quantitative angiography was used to measure minimum lumen diameter of proximal and distal coronary artery segments at baseline, during intracoronary infusion of acetylcholine (10(-7) - 10(-3) mol/l), and following an intracoronary bolus (2 mg) of isosorbide dinitrate. PATIENTS: Coronary arteriograms were obtained in 15 patients (mean (SEM) age 48 (10) years) with normal coronary arteries and chest pain. MAIN RESULTS: In response to the low concentrations of acetylcholine (10(-7) - 10(-6) mol/1) 20 (61%) distal and 11 (41%) proximal segments showed dilatation (group 1), whereas 13 (39%) distal segments and 14 (52%) proximal segments showed constriction (group 2) (P < 0.05 v group 1). In group 1, the maximum dilatation induced by acetylcholine in the proximal and distal segments was 7.83 (1.19)% and 11.6 (2.2)% respectively. In group 2, the maximum constriction at higher concentration was 16.55 (3.3)% and 33.11 (11.63)% in the proximal and distal segments respectively. The two different patterns of the vasomotor response coexisted in eight (53%) of the 15 patients. Intracoronary isosorbide dinitrate caused a greater increase in the coronary luminal diameter of distal segments than in proximal segments in group 1 (25.63 (5.16)% v 12.43 (3.48)%, P < 0.01) but not in group 2 (12.65 (2.53)% v 10.82 (3.33)%. CONCLUSIONS: Constriction and dilatation may occur in proximal and distal coronary artery segments, suggesting local areas of endothelial dysfunction, in response to acetylcholine in patients with chest pain and angiographically normal coronary arteries.

Acetylcholine↗
PubMed1996

Angiotensin II and contraction of isolated myocytes from human, guinea pig, and infarcted rat hearts.

The effects of angiotensin II on myocardial contractility were assessed in isolated cardiac myocyte preparations, using video microscopy with a computerized edge-detection system. Angiotensin II (1 nM-10 microM) did not affect the contraction of rat (n = 10), guinea pig (n = 11), or human ventricular myocytes (n = 8) or of human atrial myocytes (n = 12). Isoproterenol or raised extracellular calcium increased the contraction amplitude of the cardiac myocytes to a maximum of between 150 and 560% above basal, and there were corresponding increases in the velocities of contraction and relaxation. In rat and guinea pig ventricular myocytes 1 microM angiotensin II did not affect the inotropic response to isoproterenol. Seven days after left coronary artery ligation in seven rats, the basal contraction amplitude was reduced in myocytes from the infarcted region (4.0 +/- 1.9%) compared with the noninfarcted region (5.0 +/- 2.8%, P = 0.03) and with myocytes from six sham-operated hearts (5.0 +/- 2.8%, P = 0.03). There was a switch in myosin isoform expression from the V1 to the V3 isoform in myocytes from both the infarcted and noninfarcted regions. Angiotensin II (1 nM-10 microM) had no significant effect on the contraction characteristics of myocytes from the infarcted rat hearts. In conclusion, angiotensin II had no significant inotropic effect on isolated cardiac myocyte preparations from guinea pig ventricle, normal and infarcted rat ventricle, human ventricle, and human atrium.

Adult↗
PubMed1994

Reduced coronary vasodilator function in infarcted and normal myocardium after myocardial infarction.

BACKGROUND: The ability of the coronary vascular bed to dilate and thus increase blood flow to the myocardium may be impaired in coronary artery disease, even in regions of myocardium supplied by an angiographically normal coronary artery. If this kind of vasomotor dysfunction was present or accentuated after acute myocardial infarction, it might influence the extent of ischemia and necrosis in areas not directly injured by the infarction. METHODS: We studied 13 patients (mean [+/- SD] age, 62 +/- 11 years) with single-vessel coronary artery disease after they had received thrombolytic therapy for myocardial infarction. Using positron-emission tomography (PET) with oxygen-15-labeled water, we measured regional myocardial blood flow under basal conditions and after the intravenous administration of dipyridamole (0.5 mg per kg of body weight over a period of four minutes) 8 +/- 3 days after infarction in all 13 patients (1-week study) and 6 +/- 2 months after infarction in 9 of the 13 (6-month study). On both occasions we measured blood flow both in the infarcted region and in a region of myocardium that was remote from the infarcted region and supplied by a normal artery. RESULTS: At the one-week PET study, the coronary vasodilator response (the ratio of the myocardial blood flow after the administration of dipyridamole to basal blood flow) was 1.12 +/- 0.50 in the infarct-related artery and 1.53 +/- 0.36 in the remote region (P = 0.015). At the six-month study, the coronary vasodilator response was 1.42 +/- 0.37 in the infarcted region and 2.19 +/- 0.69 in the remote region (P = 0.004 for the comparison with the infarcted region; P = 0.011 for the comparison with the remote region at the one-week study). The value in remote myocardium remained lower than that in similar regions in 10 control patients, who had single-vessel coronary artery disease but no evidence of myocardial infarction (3.17 +/- 0.72; P = 0.009). CONCLUSIONS: After acute myocardial infarction, there is a severe vasodilator abnormality involving not only resistance vessels in infarcted myocardium, but also those in myocardium perfused by normal coronary vessels. This dysfunction may affect the extent of myocardial ischemia and necrosis after coronary occlusion.

Adult↗
PubMed1994

Left ventricular function and coronary artery disease progression early after coronary bypass grafting.

To investigate the effects of coronary artery disease progression on left ventricular function in patients who suffer angina early after coronary artery bypass grafting, we studied the progression of coronary stenoses, the occurrence of graft occlusions, and measured left ventricular ejection fraction (regional and global) in 34 consecutive patients who underwent repeat angiography 25.2 +/- 3.5 (standard error of the mean) months postoperatively, from a total population of 550 patients who underwent bypass grafting. Resting left ventricular function and stenosis severity were assessed using a computerized, quantitative analysis system. Coronary stenosis progression was defined as an increase in the percentage of the stenotic occlusion by 30% or more, any increase in lesion severity that resulted in total coronary artery occlusion, or the occurrence of a new stenosis that occluded the artery by 50% or more. Group 1 comprised 21 patients with all grafts patent and group 2 comprised 13 patients with one or more grafts occluded (20 of 34 grafts). Coronary artery disease progressed in all patients in group 1, and this involved 22 of 54 (41%) grafted vessels and 3 of 15 (20%) nongrafted vessels (p < 0.05). Coronary artery disease progressed in 11 patients in group 2, involving 15 of 32 (47%) grafted vessels and 1 of 6 (17%) nongrafted vessels (p < 0.01). An increased collateral circulation was observed in both groups. The left ventricular ejection fraction remained unchanged in both groups (group 1, 0.60 +/- 0.03 versus 0.62 +/- 0.03; group 2, 0.62 +/- 0.05 versus 0.62 +/- 0.04 before and after bypass, respectively; p = not significant) and there was no difference between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Ventricular tachycardia: an unusual pacemaker-mediated tachycardia.

A 74 year old man had recurrent ventricular tachycardia, which was well controlled with amiodarone, and complete heart block for which a VVI permanent pacing system had previously been implanted. After an elective increase in the programmed pacemaker rate from 70 to 82 beats/min, there was recurrence of frequent episodes of ventricular tachycardia. Each episode of tachycardia was initiated by a fusion beat consisting of a ventricular extrasystole and a paced beat. When the pacemaker rate was reprogrammed to 70 beats/min the episodes of tachycardia ceased abruptly. It is proposed that the fusion of a ventricular extrasystole with a pacemaker beat may have induced ventricular tachycardia, even though neither of these beats occurring separately was sufficient to cause this.

Aged↗
PubMed1993

Left ventricular hypercontractility and ST segment depression in patients with syndrome X.

OBJECTIVES: This study was designed to assess the relation between rest left ventricular function and exercise capacity in patients with syndrome X. BACKGROUND: Clinical observation has suggested that some patients with syndrome X have a high rest left ventricular ejection fraction. In this study we determined the relation between left ventricular ejection fraction and exercise capacity and the electrocardiographic (ECG) changes that develop on exercise. METHODS: The pattern of left ventricular function, exercise capacity and 24-h ambulatory ECG monitoring were studied in 37 patients (9 men, 28 women; mean age 52 +/- 7 years) with syndrome X (angina with normal coronary arteries and a positive exercise test result). All patients had normal findings on echocardiogram and rest ECG. All treatment was discontinued for > or = 48 h. Left ventricular ejection fraction was determined by computerized analysis of the left ventricular angiogram. In patients with syndrome X, exercise duration and heart rate were measured at 1-mm ST segment depression and at peak exercise. RESULTS: Left ventricular hypercontractility (ejection fraction > or = 80%) was observed in 12 patients (32%) (group 1), whereas 25 patients (68%) had normal left ventricular contraction (group 2). The time to 1-mm ST depression on exercise testing was significantly earlier in group 1 than in group 2 (5.13 +/- 1.03 vs. 10.76 +/- 0.63 min, respectively, p < 0.001). The magnitude of the ST segment depression at peak exercise was significantly greater in group 1 than in group 2 (2.03 +/- 0.2 vs. 1.33 +/- 0.05 mm, respectively, p < 0.001). The mean time for ST segment depression to normalize was significantly greater in group 1 than in group 2 (4.76 +/- 0.78 vs. 3.16 +/- 0.39 min, respectively, p < 0.05). Linear regression analysis of all patients with syndrome X showed a significant correlation between exercise duration and ejection fraction (r = 0.55, p < 0.001). The mean circadian variation of heart rate and episodes of ST segment depression on 24-h ambulatory ECG monitoring were similar in the two groups of patients. CONCLUSIONS: These findings indicate that approximately one third of patients with chest pain, normal coronary angiograms and a positive exercise test have left ventricular hypercontractility, and this is associated with the development of ST segment depression at a lower heart rate and work load and a longer time to normalization of ST segment depression after exercise.

Adult↗
PubMed1993

Diffuse reduction of myocardial beta-adrenoceptors in hypertrophic cardiomyopathy: a study with positron emission tomography.

OBJECTIVES: This study was conducted to determine the myocardial beta-adrenoceptor density as a marker of sympathetic function in patients with hypertrophic cardiomyopathy and normal control subjects. BACKGROUND: Although some cases of hypertrophic cardiomyopathy are familial with an autosomal dominant pattern of inheritance, there remains a substantial proportion of cases in which neither a family history nor genetic abnormalities can be demonstrated. Additional abnormalities, both genetic and acquired, may be important in the phenotypic expression of this condition. Clinical features of the disease and metabolic studies suggest an increased activity of the sympathetic nervous system. METHODS: Eleven patients with hypertrophic cardiomyopathy, none of whom had previously received beta-blocking drugs, and eight normal control subjects underwent positron emission tomography to evaluate regional left ventricular beta-adrenoceptor density and myocardial blood flow using carbon-11-labeled CGP 12177 and oxygen-15-labeled water as tracers. Plasma catecholamines were also measured. RESULTS: Mean (+/- SD) myocardial beta-adrenoceptor density was significantly less in the hypertrophic cardiomyopathy group than in the control group (7.70 +/- 1.86 vs. 11.50 +/- 2.18 pmol/g tissue, p < 0.001). Myocardial blood flow was similar in both groups (0.91 +/- 0.22 vs. 0.91 +/- 0.21 ml/min per g, p = NS). The distribution of beta-adrenoceptor density was uniform throughout the left ventricle in both groups. In the hypertrophic cardiomyopathy group, there was no correlation between regional wall thickness and myocardial beta-adrenoceptor density. There were no significant differences in either plasma norepinephrine or epinephrine concentrations between the two groups. CONCLUSIONS: There is a diffuse reduction in myocardial beta-adrenoceptor density in patients with hypertrophic cardiomyopathy in the absence of significantly elevated circulating catecholamine concentrations. This most likely reflects downregulation of myocardial beta-adrenoceptors secondary to increased myocardial concentrations of norepinephrine and is consistent with the hypothesis that cardiac sympathetic drive is increased in this condition.

Adult↗
PubMed1993

Delayed recovery of coronary resistive vessel function after coronary angioplasty.

OBJECTIVES: The aim of this study was to use Doppler catheterization and sequential dynamic positron emission tomography (PET) to investigate the role and time course of abnormal coronary resistive vessel function in the impairment of the coronary vasodilator response (maximal/basal coronary blood flow) after successful coronary angioplasty. BACKGROUND: The coronary vasodilator response may be impaired immediately after coronary angioplasty, despite successful dilation of a flow-limiting stenosis. METHODS: Twelve men (mean age 52 +/- 10 years) with single-vessel coronary artery disease and normal left ventricular function were studied. The coronary vasodilator response to intravenous dipyridamole (0.5 mg.kg-1 over 4 min) was determined from intracoronary Doppler measurement of coronary flow velocity, before and after successful angioplasty. Basal and maximal myocardial blood flow in the angioplasty region and a normal region were determined in nine patients wtih positron emission tomography with H2(15)0 at 1 day (PET1), 7 days (PET2) and 3 months (PET3) after angioplasty. RESULTS: The coronary vasodilator response, measured by Doppler catheterization, was similar before and immediately after angioplasty, 1.63 +/- 0.41 and 1.62 +/- 0.55, respectively (p = NS). After angioplasty, in seven of nine patients without restenosis, basal myocardial blood flow at PET1, PET2 and PET3 was 0.98 +/- 0.16, 0.94 +/- 0.09 and 0.99 +/- 0.13 ml.min-1 x g-1, respectively, in the remote region and 1.19 +/- 0.23 (p < 0.01 vs. remote region), 1.17 +/- 0.19 (p < 0.01 vs. remote region) and 1.10 +/- 0.08 ml.min-1 x g-1 (p = NS vs. remote region), respectively, in the angioplasty region. Myocardial blood flow after dipyridamole at PET1, PET2 and PET3 was 3.04 +/- 0.68, 3.00 +/- 0.71 and 3.00 +/- 0.60 ml.min-1 x g-1, respectively, in the remote region and 2.11 +/- 0.80 (p < 0.01 vs. remote region), 2.28 +/- 0.73 (p = NS vs. remote region) and 3.06 +/- 0.86 ml.min-1 x g-1 (p = NS vs. remote region), respectively, in the angioplasty region. The coronary vasodilator response at PET1, PET2 and PET3 was 3.15 +/- 0.85, 3.18 +/- 0.68 and 3.08 +/- 0.75, respectively, in the remote region and 1.80 +/- 0.68 (p < 0.01 vs. remote region), 1.94 +/- 0.49 (p < 0.01 vs. remote region) and 2.77 +/- 0.74 (p = NS vs. remote region), respectively, in the angioplasty region. CONCLUSIONS: After successful angioplasty, basal myocardial blood flow is increased for > or = 7 days in the angioplasty region, with a reduction in the dipyridamole-induced increase in maximal myocardial blood flow for > or = 24 h after the procedure. Thus, the coronary vasodilator response is impaired for > or = 7 days after angioplasty, indicating that there is abnormal resistive vessel function in the coronary vascular bed distal to a coronary artery stenosis that persists for 7 days to 3 months.

Angioplasty, Balloon, Coronary↗
PubMed1993

Variability of coronary blood flow reserve assessed by Doppler catheter after successful thrombolysis in patients with acute myocardial infarction.

To establish whether abnormal function of small coronary vessels might limit the advantages of thrombolytic treatment, coronary flow reserve in the infarct-related artery was measured in nine patients with acute myocardial infarction early after successful coronary thrombolysis by using a Doppler catheter and intracoronary adenosine infusion. In each patient coronary flow reserve was calculated as the ratio between coronary blood flow velocity during the highest tolerated intracoronary dose of adenosine (0.5 mg/min in five patients and 1 mg/min in four patients) and baseline velocity. Coronary flow reserve ranged from 1 to 3 (mean 2 +/- 0.7). No correlation (r = 0.20; p = 0.58) was found between coronary flow reserve and the severity of residual coronary stenosis, which ranged between 23% and 76% (mean 47% +/- 17%). No correlation (r = 0.33; p = 0.39) was found between either coronary flow reserve and the interval between pain onset and administration of the thrombolytic treatment, which ranged between 2.2 and 6 hours (mean 4.2 +/- 1.4 hours). Thus, in patients with acute myocardial infarction, coronary flow reserve early after successful thrombolysis is strikingly variable and may be extremely low despite widely patent epicardial coronary arteries. This restriction of coronary blood flow, probably caused by abnormal function of small coronary vessels, might limit the potential benefit from successful coronary thrombolysis.

Adenosine↗