Biomedical subjects

M Penco

Publications and source records attributed to M Penco.

At least 55 records · Page 3Linked to original sources

PubMed1994

Influence of residual perfusion within the infarct zone on the natural history of left ventricular dysfunction after acute myocardial infarction: a myocardial contrast echocardiographic study.

OBJECTIVES: This study used myocardial contrast echocardiography to investigate the extent of residual perfusion within the infarct zone in a select group of patients with recently reperfused myocardial infarction and evaluated its influence on the ultimate infarct size. BACKGROUND: Limited information is available on the status of myocardial perfusion within postischemic dysfunctional segments at predischarge and on its influence on late regional and global functional recovery. METHODS: Twenty patients with acute myocardial infarction were selected for the study. Patients met the following inclusion criteria: 1) single-vessel coronary artery disease; 2) patency of infarct-related artery with persistent postischemic dysfunctional segments at predischarge; 3) stable clinical condition up to 6 months after hospital discharge. All selected patients underwent coronary angiography and myocardial contrast echocardiography before hospital discharge and repeated the echocardiographic examination 6 months later. Patients were grouped according to the pattern of contrast enhancement in predischarge dysfunctional segments. RESULTS: In nine patients (group I), the length of segments showing abnormal contraction coincided with that of the contrast defect segments. In the remaining 11 patients (group II), postischemic dysfunctional segments were partly or completely reperfused. There was no difference between the two groups in asynergic segment length at predischarge (7.3 +/- 2.5 vs. 7.2 +/- 4.3 cm, p = NS). At follow-up study, asynergic segment length was significantly reduced in group II patients, whereas no changes were observed in group I patients (from 7.2 +/- 4.3 to 4.7 +/- 3.7 cm, p < 0.005; and from 7.3 +/- 2.5 to 7.5 +/- 2.9 cm, p = NS, respectively). CONCLUSIONS: Among patients with a predischarge patent infarct-related artery, further improvement in regional and global function may be expected during follow-up when residual perfusion in the infarct zone is present.

Adult↗

PubMed1994

IPO-V2: a prospective, multicenter, randomized, comparative clinical investigation of the effects of sulodexide in preventing cardiovascular accidents in the first year after acute myocardial infarction.

OBJECTIVES: This study was conducted to assess the efficacy of sulodexide, a glycosaminoglycan compound with antithrombotic properties, in preventing death and thromboembolic events after acute myocardial infarction. BACKGROUND: Antithrombotic therapy has been found to play an important role in the prevention of cardiovascular events and death after acute myocardial infarction. Glycosaminoglycan-containing compounds, including sulodexide, show profibrinolytic and antithrombotic properties that render them suitable for use in patients after infarction. METHODS: A total of 3,986 patients who had recovered from acute myocardial infarction were randomized to receive either the standard therapy routinely administered at each study center, excluding antiplatelet and anticoagulant drugs (control group, 1,970 patients), or the standard therapy plus sulodexide (treated group, 2,016 patients). Between 7 and 10 days after the episode of acute myocardial infarction, sulodexide was administered as a single daily 600-lipoprotein-lipase-releasing unit (LRU) intramuscular injection for the 1st month, followed by oral capsules of 500 LRU twice daily. Patients were evaluated for > or = 12 months. RESULTS: At the end of the study, 140 deaths (7.1%) were recorded in the control group and 97 (4.8%) in the sulodexide group (32% risk reduction, p = 0.0022, chi-square test). A total of 90 patients (4.6%) in the control group had a further infarction, compared with 66 (3.3%) in the sulodexide group (28% risk reduction, p = 0.035). Furthermore, a reduction in left ventricular thrombus formation (evaluated by echocardiography) was observed in the sulodexide group (n = 12; 0.6%), compared with values in the control group (n = 25; 1.3%) (53% risk reduction, p = 0.027). Sulodexide was well tolerated and devoid of significant adverse events. All significant results were confirmed by "actual treatment" analyses. CONCLUSIONS: The study provides evidence that long-term therapy with sulodexide started early after an episode of acute myocardial infarction is associated with reductions in total mortality, rate of reinfarction and mural thrombus formation.

Aged↗

PubMed1994

[Transesophageal stress echocardiography].

The Authors analyze the literature data on transesophageal stress echocardiography and personal experience with dipyridamole echocardiography. Advantages and limitations for the clinical application of this method are discussed taking into account computer-aided echocardiographic images. Transesophageal stress echocardiographic results are compared with those obtained by other stress test imaging techniques.

Echocardiography, Transesophageal↗

PubMed1994

[ACE-inhibitors after infarction: current knowledge and future prospects].

Experimental and clinical findings showing a beneficial effect on ventricular remodelling have led to a widespread use of ACE-inhibitors in myocardial infarction. Recent trials (SAVE, AIRE, GISSI 3, ISIS 4) have clearly demonstrated that in patients with left ventricular dysfunction and/or heart failure the treatment with ACE-inhibitors is mandatory, although several questions remain unanswered. Recent experimental observations on the relationship between ACE and endothelial function, and between ACE and intimal proliferation have gone forward leading to new perspectives on the potential use of ACE-inhibitors in all patients with acute myocardial infarction.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1994

[Supraventricular hyperkinetic arrhythmias in acute myocardial infarct: their prognostic assessment and correlation with the echocardiographic evolution].

To assess the prognostic significance of supraventricular tachyarrhythmias (SVTA) during acute myocardial infarction (AMI), we studied 388 patients with first AMI, without ventricular preexcitation or chronic atrial fibrillation. The prevalence of SVTA was 14% (56/388), including atrial fibrillation (57%), atrial flutter (22%), polyfocal atrial tachycardia (14%), monofocal atrial tachycardia (7%). The arrhythmia appeared within 72 hours from the onset of chest pain in 61% of patients (early SVTA < 72 hours), while in 39% appeared later (late SVTA > 72 hours). Patients with SVTA (Group I n = 56) and without SVTA (Group II n = 232) were similar regarding prevalence of hypertension, dyslipidemia, diabetes, site of infarction and fibrinolysis, but SVTA was associated with a significant increase in death (Group I 18% versus Group II 9%; p < 0.05) and complications as pulmonary oedema and cardiogenic shock (Group I 25% versus Group II 14%; p < 0.05). Left atrial dimensions (LAD), end-diastolic left ventricular volume (EDLVV), end-systolic left ventricular volume (ESLVV) and echo-score, evaluated at admission, were not different between Group I and II (LAD 41.3 +/- 6 mm versus 40.1 +/- 5 mm, NS; EDLVV 181 +/- 34 ml versus 173 +/- 30 ml, NS; ESLVV 80 +/- 21 ml versus 75 +/- 18 ml, NS; echo-score 6.7 +/- 3.1 versus 6 +/- 2.7, NS) while pre-discharge echo-grams in Group I showed a trend towards the increase in volumes and echo-score (EDLVV from 181 +/- 34 ml to 194 +/- 36 ml, p = 0.052; ESLVV from 80 +/- 23 ml to 88 +/- 23 ml, p = 0.051; echo-score from 6.7 +/- 3.1 to 7.8 +/- 3.3, p = 0.070).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1993

Influence of reperfusion induced by thrombolytic treatment on natural history of left ventricular regional wall motion abnormality in acute myocardial infarction.

Although several studies have investigated left ventricular (LV) function after reperfusion interventions, it is still unclear whether benefits result from successful therapy or whether such benefits only reflect the natural history of a subgroup of patients with acute myocardial infarction (AMI). This study evaluates the unique effect of thrombolytic therapy on the natural history of regional LV wall motion dysfunction. One hundred seventy-six patients with AMI were studied: 82 patients (group A) underwent conventional treatment and 94 (group B) thrombolytic therapy. LV regional improvement, evaluated by changes in echo score between admission and predischarge examination, was present more frequently in group B (28%) than in group A (17%). Furthermore, improved patients in group B had higher admission echo scores (7.5 +/- 3.5 vs 6.3 +/- 3.1), a prevalence of anterior AMI (68 vs 30.1%) and a higher rate of coronary patency (92 vs 58% in patients who had no improvement). In group A patients the rate of coronary patency was similar in those who did (46.1%) and did not have (36.1%) improvement. Observations at 12 to 18 months showed similar data in group A patients and in group B patients without improvement, whereas a marginal additional improvement was observed in group B patients who had in-hospital improvement. These observations demonstrate that LV function recovery is more frequent and marked in treated than in untreated patients. Follow-up results suggest a prolonged beneficial effect of thrombolytic treatment on LV function. The highest rate of coronary patency in improved group B patients underline the role of reperfusion on natural history of LV dysfunction after AMI.

Coronary Angiography↗

PubMed1993

Effectiveness of thrombolysis is associated with a time-dependent increase of malondialdehyde in peripheral blood of patients with acute myocardial infarction.

By using a highly sensitive, high-performance liquid chromatographic technique, plasma values of malondialdehyde (MDA), adenosine and oxypurines were determined in 10 healthy subjects, 10 patients with noncardiac illness, and 20 patients with acute myocardial infarction (AMI) observed within 6 hours from the onset of symptoms. Patients with AMI received fibrinolytic treatment. Peripheral blood was obtained before and serially after thrombolysis (1, 2, 3, 6 and 24 hours). Coronary patency was assessed by timing of peak creatine phosphate kinase and by predischarge angiography. MDA (mean +/- SD) in healthy subjects, noncardiac patients, and immediately before thrombolytic treatment in patients with AMI was 0.051 +/- 0.013, 0.066 +/- 0.020 and 0.397 +/- 0.326 mumol/liter of plasma, respectively. A progressive increase in plasma MDA after thrombolysis was observed only in reperfused patients, whose values at the third, sixth and 24th hours were also significantly greater than those of nonreperfused patients. Time-dependent variations of xanthine and adenosine were also observed in the same group after thrombolysis. The data appear to indicate that a relevant increase in plasma MDA, mostly originating due to phospholipid derangement of postischemic myocytes, occurs only in patients with successful thrombolysis, thus suggesting that if properly assayed, it may represent reliable biochemical evidence of tissue injuries after myocardial reperfusion in humans.

Adenosine↗

PubMed1993

[Myocardial protection: a look to the future].

Three main types of damage induced by ischemia and reperfusion have been identified: lethal reperfusion injury, microvascular and macrovascular reperfusion injury, and myocardial stunning. Pathophysiological and therapeutic aspects of these ischemia/reperfusion sequelae are reviewed and discussed on the light of recent experimental and clinical results.

Adrenergic beta-Antagonists↗

PubMed1993

[The role of compromised regional function of the left ventricle in the evolution of postinfarct ventricular thrombosis].

Five hundred twenty-nine patients with acute myocardial infarction (AMI) underwent clinical, enzymatic and echocardiographic evaluation. Two-dimensional echocardiography identified 71 patients with left ventricular thrombus (LVT): 63 males and 8 females; mean age 54 +/- 12 years; 70 with anterior AMI and 1 with inferior AMI. The incidence of LVT was 13.8% and 27.7% among anterior AMI. At admission to Coronary Care Unit the patients with LVT showed more extensive left ventricular dysfunction than patients without LVT: Killip classification > or = 2 was 54.5% versus 41.4%, p < 0.05; peak of creatinphosphokinase was 1337 UI/L versus 951 UI/L, p < 0.05; echo-score was 7.2 +/- 2.8 versus 4.7 +/- 3.5, p < 0.01. Serial echocardiograms showed disappearance of LVT in 24 patients. Regarding regional wall motion abnormalities, patients with LVT disappearance showed lower pre-discharge echo-scores than patients with LVT persistence (6.7 +/- 2.2 versus 8.4 +/- 2.9; p < 0.01) although echo-scores at admission were similar in the 2 groups (7.1 +/- 1.1 versus 7.3 +/- 3.4, NS). These results suggest: the importance of extension of myocardial infarction and left ventricular dysfunction in LVT evolution; the importance of treatment limiting infarct size and improving left ventricular function, such as thrombolytic therapy. Anticoagulant therapy could be limited to patients with higher risk of embolization (as the protruding shape of LVT).

Chi-Square Distribution↗

PubMed1993

[The variability of the heart rate in patients with a myocardial infarct undergoing systemic fibrinolysis interventions].

Although heart rate variability is a very important prognostic factor in patients with myocardial infarction, the mechanism for the reduction in the vagal cardiac activity is unknown: myocardial infarction can cause local areas of sympathetic or parasympathetic denervation that leads to catecholamine hypersensitivity; the destruction of local ventricular receptors of the autonomic system may alter feedback to the higher centres, impairing autonomic regulation; the mechanical distortion consequent to the infarction can give rise to sympathetic overactivity. Effective thrombolysis in myocardial infarction could reduce myocardial necrosis and, therefore, cause less reduction of vagal activity and/or less sympathetic stimulation. To determine whether systemic thrombolysis has some effect on heart rate variability we studied 40 patients with a first transmural myocardial infarction. Enrollment criteria were very strict: all the patients with conditions potentially influencing heart rate variability were excluded from this study. Between day 15 and day 25 from the infarction patients had an Holter monitoring. A program we developed provided for the automatic identification of R wave, for the calculation of RR interval, and for the recognition of pause, extrasystolic and post-extrasystolic beats, that could be thus excluded from the analysis. Patients were divided in 2 groups: 17 patients treated with thrombolysis and 23 subjects treated traditionally. There were no difference between the 2 groups with regard to the age and cardiac function, except for the less echo score in the fibrinolytic treated group.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocardiography, Ambulatory↗

PubMed1992

Transesophageal dipyridamole echocardiography for diagnosis of coronary artery disease.

The value of transthoracic dipyridamole echocardiography has been extensively documented. However, in some patients, because of a poor acoustic window, the rest transthoracic examination is not always feasible and the transesophageal approach is more convenient. Therefore, transesophageal echocardiography with high dose dipyridamole (up to 0.84 mg/kg body weight over 10 min) was performed in 32 patients in whom the transthoracic dipyridamole test either was not feasible (n = 29) or yielded ambiguous results (n = 3). The transesophageal echocardiographic test results were considered abnormal when new dipyridamole-induced regional wall motion abnormalities were observed. All 32 patients underwent coronary angiography; significant coronary artery disease was defined as greater than or equal to 70% lumen diameter narrowing in at least one major vessel. All patients also performed a bicycle exercise test 1 day before transesophageal dipyridamole echocardiography. Transesophageal stress studies were completed in all patients, with a maximal imaging time (in tests with a negative result) of 20 min. No side effects or intolerance to drug or transducer was observed. The left ventricle was always visualized in the four-chamber and transgastric short-axis views. High quality two-dimensional echocardiographic images were obtained in all patients both at rest and at peak dipyridamole infusion and were digitally analyzed in a quad-screen format. Coronary angiography showed coronary artery obstruction in 24 patients: 6 had single-, 9 double- and 9 triple-vessel disease. The transesophageal dipyridamole test showed a specificity of 100% and an overall sensitivity of 92%. The sensitivity of this test for single-, double- and triple-vessel disease was 67%, 100% and 100%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Angiography↗

PubMed1992

Endogenous opioid system modulation in anginal pain: demonstration of its central activity.

Plasma beta-endorphin levels provide controversial results on the role of endogenous opioid system in modulation of anginal pain. As an alternative, the action of plasmatic luteinizing hormone after administration of naloxone was investigated: naloxone blocks the tonic endogenous opioid system inhibition of gonadotropin release; thus, the level of luteinizing hormone after naloxone administration is an index of central endogenous opioid system activity. Twenty patients with coronary artery disease and positive results of stress tests were selected: 10 had angina (group I) and 10 did not (group II). Ten healthy subjects were also studied as a control group (group III). In all patients basal plasma beta-endorphin levels, basal luteinizing hormone plasma levels (every 15 minutes for 1 hour) and luteinizing hormone plasma levels after administration of 0.1 mg/kg naloxone over 4 minutes (every 15 minutes for 2 hours) were determined. In 15 patients the test was performed after luteinizing hormone releasing hormone was given. The integral concentration time of luteinizing hormone plasma level during baseline (LHiB) and after administration of naloxone (LHiN) or luteinizing hormone releasing hormone (LHiRH), the ratio (LHiN:LHiB and LHiRH:LHiB) and the differences (LHiN-LHiB and LHiRH-LHiB) between the postinfusion period and baseline were calculated. No difference was found in beta-endorphin plasma levels and luteinizing hormone response after luteinizing hormone releasing hormone infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1991

Assessment of severity of coronary narrowings by quantitative exercise echocardiography and comparison with quantitative arteriography.

To determine the correlation of quantitative assessment of coronary narrowings with left ventricular functional impairment induced by exercise, 57 patients with 1-vessel coronary artery disease and without evidence of collateral flow were studied. A significant relation was observed between minimal cross-sectional area, percent area stenosis, minimal lumen diameter, percent diameter stenosis and the percentage of segmental area change from rest to peak exercise in a vascular distribution territory (r = 0.76, p less than 0.001; r = -0.55, p less than 0.001; r = 0.56, p less than 0.001; r = -0.75, p less than 0.001, respectively). For minimal cross-sectional area, the best cut-off value to separate significantly patients who had a decrease in contractility at peak exercise testing from those who had a normal response was 2 mm2 (p less than 0.001); for percent cross-sectional area stenosis, it was 75% (p less than 0.001); for minimal lumen diameter, it was 0.7 mm (p less than 0.001); and, for percent diameter stenosis, it was 85% (p less than 0.001). High cut-off values for angiographic variables are necessary to separate significantly patients who have a decrease in contractility at peak exercise testing from those who have a normal response. Several patients with mild coronary stenoses may have either normal or abnormal wall motion during exercise. Thus, exercise echocardiography is a useful tool in detecting the presence of fairly severe anatomic narrowing, whereas it is of limited clinical use in the assessment of intermediate coronary atherosclerotic lesions.

Cineangiography↗

PubMed1991

[Noninvasive determination of anaerobic threshold: validation of an automatic computerized method].

The Authors propose a computerized method in order to automatically detect the anaerobic threshold by the analysis of ventilatory parameters (VE, VO2). The algorithm calculates all possible linear fits and the relative standard error of the relationship between VE and VO2 beginning from the first set of 4 data (excluding the first 2 min of exercise) and increasing of 1 pair of data until peak exercise. Subsequently the program chooses the line that fits the greatest number of data with the smallest error. The ventilatory anaerobic threshold (SA Ve) is then calculated as the point at which the relationship between VE and VO2 is no more linear (i.e. when the VE measured gets over of 2 standard errors the calculated value on the basis of the regression formula). During the first phase of the study the method was validated against invasive AT determination by arterial lactate concentration (SA La) in 14 patients (7 athletes, 7 healthy sedentary subjects) during a symptom-limited ergospirometric test (in supine position, 10 W/min until exhaustion). Subsequently we studied the method repeatability in 20 men (10 normals, 10 patients with congestive heart failure who performed 2 ergospirometric tests on separate days. The results showed a good correlation when comparing each other the VO2 (SA Ve 26.88 +/- 4.24, SA La 25.95 +/- 3.88 ml/kg/min; r = 0.88) or the onset time (SA Ve 11.8 +/- 2.42, SA La 11.61 +/- 1.8 min; r = 0.91) of anaerobic threshold determined by the 2 methods.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

[Hyperlipidemia, blood coagulation factors, hereditary familial factors and coronary atherosclerosis].

The identification of risk factors is very important for primary and secondary prevention of coronary artery disease. Among the different risk factors, the individual predisposition plays an important role. We have studied 130 patients with old myocardial infarction (Group A), 38 subjects belonging to the same family (Group B) and 147 control subjects in order to investigate: familiarity of coronary artery disease; distribution of lipids, lipoproteins and fibrinogen; distribution of these parameters in subjects with and without familiarity for coronary artery disease. Familiar forms showed similar lipemic and coagulative profiles as occasional forms. However, groups A and B showed significant variations in HDL-cholesterol, apolipoprotein A1, Apo A1/B ratio and in fibrinogen when compared with control subjects. These results confirm the important role of these factors and their genetical distribution. The importance of familiar distribution is also evident.

Blood Coagulation Factors↗

PubMed1991

Role of endogenous opioids on nociceptive threshold in patients with exercise-induced myocardial ischemia.

To evaluate whether endogenous opioids (EO) play a role in the perception of anginal pain, a randomized double blind clinical trial, using naloxone (N) and placebo (P) and measuring beta-endorphin (beta-ep) plasma levels, was performed. We studied 10 patients with angiographically assessed coronary artery disease (CAD) and stable exercise-induced myocardial ischemia (established by 2 preliminary bicycle ergometric tests) of whom 5 symptomatic (SYM) and 5 asymptomatic (ASYM) and 5 subjects without CAD as a control group (CON). On a third exercise test the beta-ep plasma level (fmol/ml) was measured at rest (SYM 5.4 +/- 2.3 vs ASYM 7.2 +/- 2.3 vs CON 6.8 +/- 2.6, NS), at peak exercise (SYM 4.4 +/- 1.8 vs ASYM 8.0 +/- 4.2 and vs CON 6.2 +/- 2.7, NS) and during recovery (SYM 7.5 +/- 4.2 vs ASYM 7.2 +/- 3.0 vs CON 6.7 +/- 2.5, NS). On 2 subsequent tests patients received N (0.2 mg/kg) or P intravenously and chest pain was evaluated on an analogue scale (score from 1 to 10). After N compared to P we observed: an increased perception of chest pain in SYM (6.8 +/- 1.5 vs 4.2 +/- 1.0; p less than 0.01) without significant changes of the ischemic threshold (total work, heart rate-blood pressure product, ST segment changes, 2D-echocardiographic wall motion abnormalities); no modifications in ASYM and CON.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1990

Usefulness of the dipyridamole-Doppler test for diagnosis of coronary artery disease.

Two-dimensional and Doppler echocardiographic studies and a hemodynamic investigation were performed during dipyridamole testing in 42 subjects (13 control subjects and 29 patients with coronary artery disease [CAD]), to evaluate the ability of dipyridamole Doppler echocardiography in identifying patients with ischemic left ventricular dysfunction. In the control group, after dipyridamole infusion, Doppler-derived parameters increased significantly from baseline (p less than 0.001). In patients with CAD, peak flow velocity, flow velocity integral and stroke volume failed to increase after dipyridamole infusion (0.89 +/- 0.21 to 0.85 +/- 0.18 m/s, difference not significant; 14 +/- 3 to 12 +/- 4 cm, difference not significant, and 56 +/- 13 to 50 +/- 14 ml/beat, p less than 0.05, respectively). Heart rate, rate pressure product, systemic vascular resistance and mean right atrial pressure had similar variations in the 2 groups. Changes in the 3 Doppler-derived parameters are closely related to the variations of peak positive dP/dt, stroke volume (thermodilution) and left ventricular end-diastolic pressure and are closely related to the coronary angiography jeopardy score and to the appearance of wall motion abnormalities. Thus, by combining Doppler and 2-dimensional echocardiography, dipyridamole-induced myocardial ischemia may be detected in a high percentage of CAD patients, providing a sensitive tool for identifying patients with high-risk coronary artery anatomy.

Adult↗

PubMed1989

Painless versus painful myocardial ischemia: different left ventricular dysfunction detected by echocardiography.

The mechanism responsible for the absence of anginal pain in patients who have episodes of both painless and painful myocardial ischemia, still remains unknown. Does the pain depend on an overstimulation of receptive structures or is this symptom the product of the excitation of a well-defined receptive system? The aim of this work is to test the first hypothesis: whether silent attacks are accompanied by the same degree of mechanical impairment as symptomatic ones. The authors compared the echocardiographic left ventricular functional behavior in the same patient (6 patients) during painful and painless myocardial ischemia. The echocardiographic changes observed during silent ischemic attacks were significantly different from those detected during symptomatic attacks. The latter were characterized by a larger extension of the ischemic myocardium and, as a consequence, by a larger functional impairment. Symptomatic and asymptomatic ischemic attacks were recorded echocardiographically in the same patient during repeated attacks on the same day, and were always clearly differentiated by the degree of wall motion abnormalities. The echocardiographic monitoring during the ischemic attack seemed to confirm that the greater functional impairment preceded the onset of pain leading to the occurrence of this symptom. Nevertheless, it was impossible to identify a threshold value above which the ischemic attack will be symptomatic. Our data seem to indicate a close relationship between painful ischemia and a higher degree of ischemic damage. Thus, in patients with predominantly painful myocardial ischemia, the extension and the severity of ischemia could play an important role in determining this symptom.

Adult↗