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Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 163 records · Page 9Linked to original sources
PubMed1995

Cardiac syndrome X: clinical characteristics and left ventricular function. Long-term follow-up study.

OBJECTIVES: Our aim was to study the clinical characteristics and evolution of symptoms and left ventricular function in a clinically homogeneous group of patients with syndrome X (angina pectoris, positive exercise test results and normal coronary arteriograms). BACKGROUND: The syndrome of angina with normal coronary arteriograms is heterogeneous and encompasses different pathogenetic entities. These characteristics may contribute to the existing controversy concerning the cause of syndrome X. METHODS: We studied 99 patients with syndrome X (78 women, 21 men; mean age +/- SD 48.5 +/- 8 years). All underwent clinical characterization, ambulatory electrocardiographic (ECG) monitoring and echocardiographic assessment of left ventricular function during a follow-up period of 7 +/- 4 years. RESULTS: The syndrome was more common in women than in men. Of the women, 61.5% were postmenopausal before the onset of chest pain. All 99 patients had exertional angina, and 41 also had rest angina. The average duration of episodes of chest pain was > 10 min in 53% of patients. Sublingual nitrate was effective for relief of pain in 42% of patients. Transient ST segment depression was observed during ambulatory ECG monitoring in 64 patients and myocardial perfusion abnormalities in 22. During the first stage of the exercise test, 32 patients had an increase > 20 mm Hg in systolic blood pressure and showed an earlier onset of ST depression and shorter exercise time than did patients whose blood pressure increased < or = 20%. During follow-up, no deaths or myocardial infarctions occurred, ventricular function was unchanged (shortening fraction 35.4 +/- 4% vs. 35.6 +/- 3%; heart failure developed in only one patient), systemic hypertension occurred in eight patients and conduction disturbances in four. Symptoms lessened in 11 patients, were variable or unchanged in 64 and worsened in 24. CONCLUSIONS: Syndrome X, as defined in this study, occurs predominantly in postmenopausal women. Patients usually have chest pain typical for angina, but conventional antianginal treatment is not often successful. Myocardial perfusion abnormalities occur in a small proportion of patients. Long-term survival is not adversely affected, and deterioration of cardiac function rarely occurs.

Adult↗
PubMed1995

Relation of severity of symptoms to transient myocardial ischemia and prognosis in unstable angina.

OBJECTIVES: This study was undertaken to compare the relative power of the severity of angina versus that of any other clinical, electrocardiographic (ECG) and angiographic findings in predicting the risk of subsequent in-hospital coronary events in patients admitted to the coronary care unit for treatment of unstable angina. BACKGROUND: The presence or absence of chest pain has traditionally been used to guide management and therapy of unstable angina. However, recent studies raised the possibility that the cumulative duration of ischemia may be an additional index of prognosis. METHODS: We studied 104 consecutive patients admitted to the coronary care unit because of unstable angina. Diaries of symptoms were accurately kept. All patients underwent Holter ambulatory ECG monitoring during the 1st 24 h and angiography within 1 week of admission. RESULTS: During the hospital stay, 41 patients (group 1) had subsequent coronary events; the remaining 63 patients (group 2) had a good clinical outcome. Recurrence of chest pain after admission was observed in 76% of patients: 36 of the 41 group 1 patients (sensitivity 88%) and 43 of the 63 group 2 patients (specificity 32%). Anginal scores (frequency and persistence of pain, duration of each single episode and pain-free interval) showed high specificity but low sensitivity for detecting evolution toward subsequent coronary events. On Holter monitoring, the duration/24 h of the total number of ischemic episodes was consistently greater in group 1 than in group 2. A cumulative duration of ischemia > or = 60 min/24 h was observed in 34 of the 41 group 1 patients (sensitivity 83%) but in only 16 of the 63 group 2 patients (specificity 75%). High risk coronary artery lesions (left main coronary artery disease or complex stenosis) were detected in 36 of the 41 group 1 patients and in 26 of the 63 group 2 patients. CONCLUSIONS: Transient myocardial ischemia detected by Holter monitoring, but not chest pain, is the best predictor of unfavorable short-term clinical outcome. The decision to perform early angiography and revascularization cannot be based on symptoms alone.

Aged↗
PubMed1995

Relation between myocardial infarction site and pain location in Q-wave acute myocardial infarction.

Location, severity, duration, and time course of pain were assessed in 104 consecutive patients with either first or second, anterior or inferior Q-wave acute myocardial infarction (AMI). Pain severity was assessed using a visual analog scale. Pain location and radiation were similar in 48 patients with anterior and 56 patients with inferior wall AMI. Pain duration (6.1 +/- 6.4 vs 6.5 +/- 5.4 hours, p = NS) and severity (68 +/- 21 vs 61 +/- 21 mm, p = NS) were also similar. The pain was continuous in 34 patients with anterior (71%) and in 42 with inferior (75%) wall AMI. Among the 41 patients who did not receive thrombolytic therapy, 18 patients with continuous pain had a higher creatine kinase peak level than the remaining 23 patients with intermittent pain or preinfarction angina, or both (2,065 +/- 1,017 vs 1,162 +/- 994 IU, p < 0.01). The incidence of gastrointestinal symptoms was slightly higher in patients with inferior than anterior wall AMI (70% vs 48%, p < 0.05). Among 32 patients admitted with a second AMI, pain location was similar in 14 who had both infarcts in the same myocardial region, but was different in 12 of 18 (67%) who had a first and second infarct in different regions (p < 0.001). Thus, patients with anterior or inferior wall AMI experienced pain in similar body regions. However, in patients who presented with > 1 AMI, different locations of the infarction pain were highly predictive of ischemia occurring in different myocardial regions. Finally, patients with preinfarction angina or intermittent pain tended to have smaller infarcts.

Adult↗
PubMed1995

Duration and magnitude of ST-segment depression during exercise and recovery: a symmetric relation.

The pattern of appearance and disappearance of ST depression on 12-lead electrocardiographic exercise testing in subjects with coronary artery disease (> or = 70% stenosis) and its relation to the severity of disease were prospectively explored in 34 consecutive patients. The first lead to show positivity during exercise also developed maximum ST depression in 73% of patients and was the last lead to lose positivity in recovery (94%). The last lead to show positivity during exercise was first to lose positivity in recovery (92%). Greater ST depression was associated with a greater number of positive leads (p < 0.001; r = 0.7). The duration of ST depression during exercise, maximum ST depression, and recovery time were related (p = 0.001, r = 0.6; p = 0.006, r = 0.5; p < 0.001, r = 0.6, respectively, for the three interactions). However, the correlations of ST depression and recovery time with the severity of vessel disease and with rate-pressure product at initial ST depression were poor, suggesting that the degree of ST-segment depression and recovery time may depend more on the duration and intensity of myocardial ischemia solicited with exercise rather than on the ischemic threshold or on the severity of coronary artery disease.

Cohort Studies↗
PubMed1995

Early spontaneous intermittent myocardial reperfusion during acute myocardial infarction is associated with augmented thrombogenic activity and less myocardial damage.

OBJECTIVES: This study investigated the influence of early spontaneous intermittent reperfusion on the extent of myocardial damage and its relation to endogenous hemostatic activity. BACKGROUND: In the early phase of acute myocardial infarction coronary occlusion is often intermittent, even before thrombolytic therapy is administered. The relation between this phenomenon, myocardial damage and hemostatic activity is unknown. METHODS: Holter ST segment recording and pretreatment plasma tissue-type plasminogen activator (t-PA) antigen, plasminogen activator inhibitor-1 (PAI-1) antigen, prothrombin fragment F1 + 2 and soluble fibrin levels were measured in 57 patients with acute evolving myocardial infarction. Spontaneous intermittent myocardial reperfusion, defined as two or more episodes of transient resolution of ST segment elevation to within 0.05 mV of baseline, lasting > or = 1 min, before the start of recombinant t-PA (rt-PA) treatment was present in 28 patients (group 1) and absent in 29 (group 2). Left ventriculography and coronary angiography were performed 90 min after intravenous rt-PA administration. Plasma creatine kinase-MB fraction (CK-MB) levels were measured every 6 h for 24 h, and C-reactive protein levels were measured daily for 3 days. RESULTS: Group 1 had lower peak plasma CK-MB (141.9 +/- 28.3 vs. 203.8 +/- 23.3 IU/liter [mean +/- SEM], p < 0.014) and C-reactive protein levels (16 +/- 4 vs. 28 +/- 4 mg/liter on day 1; 26.6 +/- 5.5 vs. 61.8 +/- 14.4 mg/liter on day 2; 19.6 +/- 4.2 vs. 40.6 +/- 6.5 mg/liter on day 3, p < 0.012) and a higher left ventricular ejection fraction (62.9 +/- 4% vs. 51.1 +/- 5%, p < 0.04) than group 2. Group 1 had lower plasma t-PA antigen levels (15.6 vs. 27 micrograms/liter, p < 0.006) but higher prothrombin fragment F1 + 2 (1.8 vs. 1.1 nmol/liter, p < 0.003) and soluble fibrin levels (66.8 vs. 31 nmol/liter, p < 0.01). Coronary patency at 90 min was similar. CONCLUSIONS: Early spontaneous intermittent reperfusion during acute myocardial infarction is associated with augmented thrombogenic activity and less subsequent myocardial damage. This finding is consistent with a protective effect of intermittency on the myocardium and a procoagulant effect of spontaneous lysis on blood. It may also reflect a different rate of evolution of coronary thrombosis and myocardial infarction in patients with and those without spontaneous intermittent myocardial reperfusion.

Analysis of Variance↗
PubMed1995

Microvascular angina in patients with normal coronary arteries and with other ischaemic syndromes.

In this paper we review the evidence that angina and 'ischaemic' ST depression can be caused by inappropriate constriction of small coronary artery vessels in patients with microvascular angina (i.e. anginal chest pain with angiographically normal coronary arteries). Although the mechanisms responsible for microvascular dysfunction remain unknown, it is conceivable that the constrictor stimuli may involve vessels which are proximal to those involved in metabolically induced dilation, so that the effect cannot be opposed, at the same site, by the dilator effect caused by ischaemic metabolites. Furthermore, in this review we also present evidence that myocardial ischaemia may result mainly from inappropriate constriction of small coronary vessels, rather than by obstruction of major epicardial coronary arteries. In addition, there are those prone to the condition, such as specific groups of patients with atherosclerotic ischaemic syndromes, including patients with single isolated coronary artery occlusion and no evidence of previous myocardial infarction, patients with single-vessel coronary stenosis who underwent successful balloon angioplasty, and patients with single-vessel disease with detectable abnormal vasomotor responses in non-stenotic coronary arteries.

Adenosine↗
PubMed1995

Hyperdynamic performance of remote myocardium in acute infarction. Correlation between regional contractile function and myocardial perfusion.

During and after myocardial infarction (MI), compensatory contractile and structural changes taking place in the remote uninvolved myocardial regions have been well described, in both experimental and clinical settings. However, quantitative information on the changes in perfusion in these regions in relation to their altered contractile function have not been available. This study was designed to assess the in vivo relationship between contractile function and perfusion in remote uninvolved hypercontractile myocardial regions, subtended by angiographically normal coronary arteries in patients with MI and single-vessel coronary artery disease. We utilized two-dimensional echocardiography and 15O-water positron emission tomography imaging to assess regional contractile function and myocardial blood flow, respectively. Measurements were performed in nine patients with single-vessel coronary artery disease and angiographically confirmed recanalization of the infarct-related artery, 1-2 days after MI (group A). Only patients demonstrating severely impaired wall motion of the infarcted area and reactive hypercontractility of the remote uninvolved regions were enrolled. Seven patients with previous non-reperfused MI (6-8 months post-MI) served as a control (group B). Systolic wall thickening and regional myocardial blood flow data sets were created for the remote myocardial segments perfused by angiographically detected patent coronary arteries by assigning regions on the tomograms to equivalent echocardiographic segments. In the remote regions, wall thickening and regional myocardial blood flow were higher in group A patients by 26% (43 +/- 6% vs 34 +/- 4%; P = 0.005) and 20% (1.06 +/- 0.15 vs 0.89 +/- 0.06 ml.g-1 per minute; P = 0.019), respectively. For both groups of patients, a significant correlation (r = 0.67; P = 0.004) between systolic wall thickening and regional myocardial blood flow was obtained. Infarcted regions in both groups showed no systolic wall thickening. In this selected group of patients these data demonstrate: (1) a proportionate increase in contractility and regional myocardial blood flow in uninvolved territories in patients with recent and old MI; (2) the in vivo relationship between contractile function and myocardial perfusion in man in these regions. When infarcted zones in both groups are equally affected, enhanced levels of catecholamines and sympathetic drive as well as different loading conditions may account for the hyperkinetic performance and consequently for the increased perfusion level in uninvolved segments in patients with recent MI.

Adult↗
PubMed1995

Endothelium-derived haemostatic factors and the antiphospholipid syndrome.

The cause of thrombosis in the antiphospholipid syndrome (APS) is unknown. There have been reports of abnormalities in the antigenic levels or activity of endothelium-derived haemostatic factors, such as tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1); however the data from these studies are conflicting. We studied plasma from nine patients with APS; seven of them had a history of thrombosis, and three had systemic lupus erythematosus (SLE). We also studied nine matched control patients who had SLE without APS, and 14 healthy individuals. We measured t-PA, von Willebrand factor (vWF), anticardiolipin antibody (ACA) and anti-endothelial cell antibody (AECA) levels by enzyme-linked immunoassay (ELISA), PAI-1 activity by a parabolic-rate chromogenic assay, and lupus anticoagulant (LA) activity by a standard mixing test. For t-PA and PAI-1, measurements were made on morning and evening plasma samples. The two groups of patients did not differ significantly with respect to age, sex, plasma lipids or anti-inflammatory drugs. Most APS patients (7/9) but none of the controls were taking warfarin. Between the APS and the control patients no significant differences were detected in t-PA, PAI-1, vWF or AECA levels. When APS patients were considered alone, vWF levels correlated positively with IgG ACA levels (r = 0.81, P < 0.01) and negatively with platelet count (r = -0.68, P < 0.05). There was no correlation between levels of ACA or LA activity and t-PA, PAI-1 or AECA. Compared with healthy volunteers, the diurnal variation of t-PA and PAI-1 was blunted in the two patient groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Early remodelling of coronary stenoses after thrombolytic treatment in patients with acute myocardial infarction.

OBJECTIVE: To assess the frequency of early remodelling of coronary stenosis morphology after thrombolytic treatment in patients with acute myocardial infarction. DESIGN: Coronary angiograms were analysed by a computerised edge detection analysis system. Coronary stenosis severity was measured and morphology classified as smooth or complex. PATIENTS: Coronary arteriograms were obtained approximately 90 min and 24 h after thrombolytic treatment from 40 patients with acute myocardial infarction. MAIN RESULTS: Stenosis morphology was complex in 22 patients (65%) and smooth in 11 (32%) 90 min after thrombolysis. The morphology of 11 (50%) complex coronary stenoses and three (27%) smooth stenoses had changed at 24 h (P < 0.05). The transition from complex to smooth was associated with a reduction in stenosis severity from 65 (4)% to 51 (5)% (P < 0.05). The stenosis severity was 63 (4)% and 60 (5)% in those with persistently complex morphology, and 56 (7)% and 50 (5)% in those with persistently smooth morphology at 90 min and 24 h respectively (NS). CONCLUSIONS: Transition of morphology from complex to smooth within 24 h is common. This transition is associated with a reduction in stenosis severity of a degree greater than that found in persistently smooth stenoses over the same interval. 50% of stenoses are smooth at 24 h.

Adult↗
PubMed1995

Differences in vasodilatory response to dipyridamole between patients with angina and normal coronary arteries and patients with successful coronary angioplasty.

BACKGROUND: Previous studies reported a reduced coronary blood flow reserve, assessed by the intravenous administration of dipyridamole, in patients with angina and normal coronary arteries, and early after successful coronary angioplasty, which suggests the presence of small coronary vessel dysfunction. This study aimed to establish whether the mechanisms of small coronary vessel disease in these two groups of patients are similar. METHODS: The effects of the intracoronary infusion of adenosine and dipyridamole (maximum dose 2.7 and 7.5 mg/min, respectively) on coronary blood flow velocity were assessed in 11 patients with angina and normal coronary arteries (group A) and in 12 patients immediately after successful coronary angioplasty (group B) using a 0.018" Doppler wire. RESULTS: Baseline coronary blood flow velocity was significantly higher in group B than group A (34 +/- 14 versus 19 +/- 8 cm/s; P = 0.001). In group A, coronary blood flow velocity was higher during adenosine than dipyridamole infusion (74 +/- 17 versus 58 +/- 21 cm/s; P < 0.001), whereas in group B velocities were similar (85 +/- 30 versus 78 +/- 32 cm/s; NS). CONCLUSIONS: In patients with angina and normal coronary arteries, a maximal dose of adenosine causes a greater coronary dilation than that of dipyridamole. Given that dipyridamole operates mainly through an inhibition of adenosine re-uptake, it can only dilate the arteriolar segments exposed to endogenous adenosine. Therefore, the lower response to dipyridamole than to exogenous adenosine observed in patients with angina and normal coronary arteries suggests an impairment of the pre-arterioles that are not influenced by endogenous adenosine, resulting in a limited flow-mediated dilation in response to arteriolar dilation. Such an impairment is not apparent immediately after successful coronary angioplasty, where the most obvious abnormality is an increase of baseline coronary blood flow velocity.

Adenosine↗
PubMed1995

[Psychological stress as precipitating factor of the acute manifestations of ischemic cardiopathy].

Psychological stress may play an important role as a risk factor for coronary heart disease (CHD). Psychological stress consists of different components whose diverse role in the onset of the acute manifestations of CHD is still not clear. We studied 80 patients with acute CHD (56 with unheralded myocardial infarction, 24 with unstable angina, mean age 55 +/- 9 years, 55 men) vs 80 controls (mean age 50 +/- 9 years, 52 men) admitted for an acute traumatic event. We proposed to both groups these questionnaires: a retrospective self and etero-evaluation of the degree of psychological stress; the modified Maastricht questionnaire (MMQ) that evaluates psychic and physical manifestations of psychological stress in the period preceding admission; the social support questionnaire (SSQ); the life event assessment that evaluates frequency and importance of life events in the year preceding admission. Psychological stress index was greater in patients (self-evaluation = 7.1 +/- 2.4; etero-evaluation = 7.4 +/- 2.3; MMQ = 91 +/- 30.8) than controls (self-evaluation = 4.3 +/- 2.3; etero-evaluation = 4.3 +/- 2.4; MMQ = 58.6 +/- 32.5; p < 0.001 for all questionnaires). The perception of strong social isolation was greater in patients (SSQ = 29.8 +/- 11.8) than controls (SSQ = 23.8 +/- 9.6; p < 0.001). Painful life events were more numerous in patients (10.7 +/- 2.3) than controls (8.2 +/- 3.4; p < 0.05) and perceived in a more negative way (patients = 12.7 +/- 4.1 vs controls = 10.2 +/- 3.8; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Case-Control Studies↗
PubMed1995

[Hemostatic factors and family history of thrombosis in patients with a myocardial infarct: a case-control study. The participants in GISSI-2-Efrim. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico].

We studied a series of hemostasis factors in a group of patients selected from a cohort of 916 patients affected by MI from the GISSI-2 study population. Following a case-control design, 73 patients with a family history of thrombosis (the presence of at least two first degree relatives affected by MI and/or stroke before 65 years) were matched with MI patients with no family history of thrombosis. Blood collection could be performed 6 +/- 1 months after the acute phase following MI in 53 pairs of such patients. The presence of mixed disulphides (MDS) was significantly higher in patients with family history than in controls; MDS were detected in 7 cases and only in 1 control. No difference was found in contrast in the distribution of fibrinogen, factor VII, factor VIII, vWF, protein C, protein S, AT III, HC II, PAI-1, lipoprotein (a). Nevertheless, independently from the family history, in the whole population of MI patients studied, 21 cases of suspected deficiency of protein C were found. Sixteen out of 53 patients with family history of MI and/or stroke had a family history of MI only. In patients with family history of MI the t-PA antigen levels were significantly lower than in the control group (7.5 +/- 4.4 vs 11.1 +/- 3.5 ng/ml, t = -2.6, p < 0.02). In the whole population of MI patients and in patients with a family history of thrombosis t-PA antigen was positively correlated with PAI-1 antigen and vWF. The correlation with PAI-1 was lost in patients with family history of MI.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

Usefulness of a third Holter lead for detection of myocardial ischemia.

Two-channel ambulatory electrocardiographic (ECG) monitoring is a useful method for detecting transient myocardial ischemia in patients with coronary artery disease. However, the monitoring of only 2 leads may fail to detect a significant number of ischemic episodes. In this study, the additional diagnostic value of a third bipolar chest lead was evaluated by recording a simultaneous 12-lead electrocardiogram and a 3-channel ambulatory electrocardiogram during exercise testing in 223 patients (aged 63 +/- 10 years) with proved or suspected coronary disease. Leads CM5, CM3, and an inferior lead (Y-modified or CMf) were monitored on the ambulatory electrocardiogram. Diagnostic ST-segment depression on the standard electrocardiogram was detected in 98 patients (44%), 94 (96%) of whom also had diagnostic ST-segment changes on the ambulatory electrocardiogram. Two additional patients had ST-segment depression only on the ambulatory electrocardiogram (both in lead CM5). Maximal ST-segment depression and duration of ischemia detected on standard and ambulatory ECG leads were similar in the 94 patients in whom ST-segment changes were detected on both types of ECG monitoring. CM5 was the single lead with the highest sensitivity (89%) in detecting myocardial ischemia. The addition of CM3 to CM5 increased sensitivity to 91%, and the addition of an inferior lead to CM5 increased sensitivity to 94%, particularly improving the detection of isolated inferior myocardial ischemia. The combination of all 3 ambulatory ECG leads had a sensitivity of 96%, an improvement of only 2% compared with the best combination of 2 leads (i.e., CM5 +/- inferior lead).(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocardiography↗
PubMed1994

The prognostic value of C-reactive protein and serum amyloid a protein in severe unstable angina.

BACKGROUND: The pathogenesis of unstable angina is poorly understood, and predicting the prognosis at the time of hospital admission is problematic. Recent evidence suggests that there may be active inflammation, possibly in the coronary arteries, in this syndrome. We therefore studied the prognostic value of measurements of the circulating acute-phase reactants C-reactive protein and serum amyloid A protein, which are sensitive indicators of inflammation. METHODS: We measured C-reactive protein, serum amyloid A protein, creatine kinase, and cardiac troponin T in 32 patients with chronic stable angina, 31 patients with severe unstable angina, and 29 patients with acute myocardial infarction. RESULTS: At the time of hospital admission, creatine kinase and cardiac troponin T levels were normal in all the patients, but the levels of C-reactive protein and serum amyloid A protein were > or = 0.3 mg per deciliter (exceeding the 90th percentile of the normal distribution) in 4 of the patients with stable angina (13 percent), 20 of the patients with unstable angina (65 percent), and 22 of the patients with acute myocardial infarction (76 percent). The 20 patients with unstable angina who had levels of C-reactive protein and serum amyloid A protein > or = 0.3 mg per deciliter had more ischemic episodes in the hospital than those with levels < 0.3 mg per deciliter (mean [+/- SD] number of episodes per patient, 4.8 +/- 2.5 vs. 1.8 +/- 2.4; P = 0.004); 5 patients subsequently had a myocardial infarction, 2 died, and 12 required immediate coronary revascularization. In contrast, no deaths or myocardial infarction occurred among the 11 patients with levels of C-reactive protein and serum amyloid A protein < 0.3 mg per deciliter, and only 2 of them required coronary revascularization. Among the patients admitted with a diagnosis of acute myocardial infarction, unstable angina preceded infarction in 14 of the 22 patients (64 percent) with levels of C-reactive protein and serum amyloid A protein > or = 0.3 mg per deciliter but in none of the 7 patients with levels < 0.3 mg per deciliter. CONCLUSIONS: Elevation of the sensitive acute-phase proteins C-reactive protein and serum amyloid A protein at the time of hospital admission predicts a poor outcome in patients with unstable angina and may reflect an important inflammatory component in the pathogenesis of this condition.

Angina Pectoris↗
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↗