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Biomedical subjects

R Bugiardini

Publications and source records attributed to R Bugiardini.

At least 19 recordsLinked to original sources
PubMed1996

Transient sympathovagal imbalance triggers "ischemic" sudden death in patients undergoing electrocardiographic Holter monitoring.

OBJECTIVES: The aim of this study was to investigate the relation between "ischemic" sudden death (arrhythmic death preceded by ST segment shift) and autonomic nervous system activity. Background. Mechanisms precipitating sudden death are poorly known despite the importance of detecting functional factors that may contribute to such a fatal event. METHODS: We analyzed the tapes of eight patients (seven men and one woman with a mean age of 66 +/- 8 years) who had ischemic sudden death during ambulatory electrocardiographic (Holter) monitoring. Four patients had unstable and four had stable angina; none was taking antiarrhythmic drugs. Twenty patients with angina and transient myocardial ischemia during Holter monitoring served as control subjects. Arrhythmias, ST segment changes and heart rate variability were analyzed by a computerized interactive Holter system. RESULTS: Five patients had ventricular tachyarrhythmias (ventricular fibrillation in three, ventricular tachycardia in two), and three had bradyarrhythmias (atrioventricular block in two, sinus arrest in one) as the terminal event; all eight patients showed ST segment shift (maximal change 0.46 +/- 0.16 mV; with ST elevation in two) that occurred 41 +/- 34 min (mean +/- SD) before sudden death. The standard deviation of normal RR intervals (SDNN) was 89 +/- 33 ms during the 10 +/- 6 h of Holter monitoring; 5 min before the onset of the fatal ST shift, SDNN measurements were significantly lower than during the initial 5-min period (48 +/- 10 vs. 29 +/- 9 ms; p=0.002). In control patients, the SDNN was 102 +/- 39 ms during Holter monitoring, whereas it measured 56 +/- 30 ms 5 min before the most significant episode of ST shift (p<0.01 vs. 29 +/- 9 ms [corrected] in the group with sudden death). CONCLUSIONS: Autonomic dysfunction, as detected by a marked decrease in heart rate variability, is present in the period (5 min) immediately preceding the onset of the ST shift precipitating ischemic sudden death. These data suggest that sympathovagal imbalance may trigger fatal arrhythmias during acute myocardial ischemia, thus resulting in sudden death.

Aged↗
PubMed1996

[The correlation between the clinical characteristics and psychological status in syndrome X patients].

Patients with anginal symptoms and normal coronary arteries have been found to present with high levels of neuroticism i.e. anxiety, depression and somatic concerns. Whether neuroticism plays a role in precipitating coronary hypoperfusion and symptoms is still a matter of investigation. The present study was undertaken to assess the relation between psychological status and clinical symptoms in 22 patients with syndrome X (angina and ST depression with angiographically normal coronary arteries and reversible myocardial perfusion abnormalities). Neuroticism was evaluated by Beck Depression Inventory, Hamilton Anxiety Rating Scale (HAM-A), State-Trait Anxiety Inventory, Sheehan Patient Rated Anxiety Scale, State-Trait Anger Expression Inventory (STAXI), Brief Psychiatric Rating Scale and Clinical Global Impression. Data were compared with those obtained in 30 patients with stable angina as well as coronary artery disease. All patients underwent an exercise stress testing and a 24-hour ambulatory Holter monitoring. Patients with syndrome X scored significantly higher than stable angina (p < 0.05 each) on all psychological tests but STAXI. No significant differences, between syndrome X and stable angina were found in exercise stress testing parameters and during Holter monitoring. Twelve out of 22 syndrome X patients had a score > 28 in HAM-A (Group 1, with frank psychiatric abnormalities). The remaining 10 patients were labelled as Group 2. No significant differences between Group 1 and Group 2 were found in exercise capacity (time to 0.1 m V ST depression: 397 +/- 73 and 419 +/- 137 s, respectively; NS) or in the number of anginal episodes per day (0.9 +/- 1.3/24 hours and 0.6 +/- 0.8/24 hours respectively; NS). In contrast, Holter monitoring showed a significantly higher number of ischemic episodes in Group 1 than in Group 2 (1.6 +/- 1.7 vs 0.1 +/- 0.3/24 hours; p < 0.02) and a greater duration of ischemia (23.8 +/- 32 vs 0.3 +/- 1 min/24 hours; p < 0.03). We conclude that: patients with syndrome X evidence elevated neuroticism scores; a high degree of anxiety correlates with increased transient myocardial ischemia during daily life; neuroticism may itself cause changes in coronary microvascular function in syndrome X. Alternatively it may simply modulate the threshold for ischemia in the presence of underlying dysfunction.

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

[A transient decrease in heart rate variability in patients with sudden "ischemic" death during Holter monitoring].

BACKGROUND: Mechanisms precipitating sudden death are poorly known, in spite of the importance to detect functional factors which may contribute to such fatal event. Aim of the study was to investigate the relationship between "ischemic" sudden death (ISD: arrhythmic death preceded by acute myocardial ischemia) and autonomic nervous system activity. METHODS: We analysed the tapes of 6 patients (pts) (5 males; 67 +/- 12 yrs) suffering ISD during Holter monitoring (HM). One pt had recent onset angina, 2 had unstable and 3 stable angina; none was taking antiarrhythmic drugs. Arrhythmias, ST segment and heart rate variability (HRV) were analysed by a computerized interactive HM system, in order to obtain data on transient ischemia and sympatho-vagal balance. RESULTS: Five pts showed ventricular tachyarrhythmias (2 VF, 3 VT), and 1 had a bradyarrhythmia (advanced A-V block) as the terminal event; all pts showed ST shift (max: 0.37 +/- 0.28 mV; 1 with ST elevation; 4 with anginal pain) 53 +/- 35 min before ISD. SD of normal R-R intervals (SDNN) was 112 +/- 26 msec in the 11 +/- 8 hrs of HM, whereas it was 97 +/- 48 msec in the initial hour and 59 +/- 21 msec in the initial 5 min segment. Measurements of SDNN showed a marked decrease 5 min before the onset of fatal ischemic ST shift: 32 +/- 14 msec (p = 0.003). Also, pNN50 (percent of adjacent R-R differing > 50 msec: marker of vagal activity) was significantly reduced before ISD, when compared to the initial 5 min segment (from 10 +/- 5 to 7 +/- 4%; p < 0.03). Such changes were not observed before uncomplicated (that is not associated with malignant arrhythmias) ST shift episodes during HM. CONCLUSIONS: Autonomic dysfunction, as detected by a marked decrease of HRV, is present in the period (5 min) immediately preceding the onset of ST shift precipitating ISD; simultaneous measurements of vagal signals showed similar changes. These data suggest that sympatho-vagal unbalance may trigger fatal arrhythmias during acute myocardial ischemia, hence resulting in ISD.

Aged↗
PubMed1995

[The noninvasive identification of patients with angina and normal coronary arteries].

BACKGROUND: Although patients with syndrome X (angina and normal coronary arteries, in absence of coronary spasm, cardiomyopathy or valvulopathy) and those with stable angina as well as documented coronary artery disease share a similar clinical presentation (effort related symptoms, positive exercise stress testing and reversible perfusion defects), their prognosis is markedly different. Coronary atherosclerosis is usually progressive relative to morbidity and mortality. Conversely prognosis both in terms of persistence of pain and mortality appears to be benign in syndrome X. Most cardiologists favor proceeding with coronary angiography in all patients presenting with exercise induced ST depression and reversible perfusion defects. However, it should not be assumed that this strategy will remain the preferred one. The aim of this study was to assess whether non invasive testing could identify underlying coronary artery anatomy, thus prognosis in the above subset of patients. The approach was selected on a clearly stated objective of how isosorbide dinitrate and verapamil may influence coronary flow reserve, thus exercise stress testing in syndrome X. Nitrates have been shown to reduce coronary flow reserve during stress tachycardia. The opposite occurs with calcium blockers. METHODS: We studied 48 patients with effort angina referred to our laboratory for diagnostic evaluation. All patients underwent two separate sessions at one-day interval. Each session consisted of exercise stress testing before and after isosorbide dinitrate (s.l.; 5-10 mg) or verapamil (i.v.; 10 mg), given in a randomized crossover fashion. Angiography was performed within 3 months from testing. Efficacy of drugs in terms of exercise capacity was assessed by using the following criteria: 1) prevention of significant (> or = 0.1 mV) ST depression while reaching same workload levels attained during baseline testing; 2) improvement in the ischemic thresholds, that is an increase in: time to 0.1 mV ST depression > or = 120 sec., with heart rate (> or = 10 bpm) and rate pressure product (> or = 2 U x 1000) greater than those attained during baseline testing; 3) increase in time to peak exercise (> or = 120 sec). RESULTS: In syndrome X, both drugs resulted ineffective in one patient, one patient showed a favourable response to isosorbide dinitrate whereas the remaining 13/15 patients improved exercise capacity following verapamil, but not isosorbide dinitrate. The opposite occurred in coronary artery disease patients: both isosorbide dinitrate and verapamil were effective in 21/33 patients, and ineffective in 8/33 patients. The remaining 4 patients responded to isosorbide dinitrate but not to verapamil. CONCLUSIONS: 1) Verapamil, but not isosorbide dinitrate, improves exercise capacity in syndrome X; 2) this does not apply to patients with stable angina; 3) a favourable response to verapamil but not to isosorbide dinitrate is both a sensitive (86%) and specific (100%) method for identifying patients with angina and normal coronary arteries; 4) non invasive testing may select those effort angina patients who have to proceed directly to coronary angiography; 5) some patients with effort related angina may not require further investigation.

Adult↗
PubMed1994

[Myocardial infarct with normal coronary vessels: an association with dysfunction of the coronary microcirculation].

The association of acute myocardial infarction (AMI) with normal coronary arteries was analyzed prospectively. A series of 128 consecutive patients underwent coronary angiography within 1 week from AMI. Seven patients, all females, had no coronary artery lesions and were considered eligible for the study. All 7 patients underwent atrial pacing (10 g/min increments every 2 min), ergonovine testing (E; total dose 0.650 mg i.v.). Great cardiac vein flow (GCVF; thermodilution technique), mean aortic pressure (MAP), anterior coronary resistance (ACR) and myocardial lactate extraction [(Lac art-Lac gcv)/Lac art] were measured at baseline and during testing. Pacing-induced typical chest pain occurred in 5 patients: 4 of them showed concurrent significant (> or = 0.15 mV) ST downsloping. At peak pacing, GCVF increased only by < 50%, or even decreased, in all patients. Baseline lactate extraction (0.13 +/- 0.11) changed to lactate production (-0.15 +/- 0.10) in 7/7 patients. None of the patients showed focal epicardial coronary artery spasm following E. During testing, however, all 7 patients showed decrease in GCVF (110 +/- 47 versus 74 +/- 21; p < 0.005), increase in ACR (0.92 +/- 0.29 versus 1.43 +/- 0.20; p < 0.001), and significant coronary lactate production (-0.18 +/- 0.12). Six patients referred slight to moderate chest pain, which was accompanied by ST downsloping in 4.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[Exudative pericarditis with pleural plaques caused by exposure to asbestos, resolved with steroidal treatment].

We report a case of a 73-year old railwayman with an asymptomatic large pericardial effusion diagnosed by a routine echocardiogram. By clinical and laboratory tests we excluded an immune, infectious, tuberculous and neoplastic origin of the pericardial effusion. A computed tomography scan of the thorax showed left pleural plaques. Pleural and pericardial biopsies showed fibrohyaline plaques and diffuse aspecific, chronic inflammation consistent with asbestos exposure. By using steroid treatment there was no further evidence of pericardial inflammation or pericardial effusion at 8 month follow-up. Steroid drugs are therefore suggested as a first choice treatment in patients with pleuropericardial effusion as well as chronic asbestos exposure.

Aged↗
PubMed1994

[An analysis of the variability of the heart rate and its significance in the risk stratification of patients with unstable angina].

Decreased heart rate variability (HRV) correlates with increased sympathetic or decreased vagal tone. This could contribute to increase local coronary hyperreactivity caused by atherosclerotic plaque disruption, thus facilitating progression from unstable angina to acute myocardial infarction (AMI). To test this hypothesis we studied 92 patients admitted to the coronary care unit for episodes of chest pain at rest associated with transient ST shifts (> 0.15 mV). Patients who developed AMI in the first 24 hours, as well as those with previous AMI, concomitant valvular or myocardial diseases or diabetes mellitus were not enrolled in the study. Thirty age-matched subjects without any evidence of coronary artery disease were chosen as controls. All patients underwent a 2 to 5 day continuous Holter monitoring during full medical treatment (including beta-blockers, heparin and aspirin). Angiography was performed within 1 week in 88 of the 92 patients. During follow-up (mean duration of 16 +/- 5 days), 26 patients (Group I) had a major coronary event (6 deaths, 7 non fatal AMI, 13 urgent revascularizations). The remaining 66 patients (Group II) had a good clinical outcome. ECG recordings during ST shifts were excluded from Holter monitoring analysis. Time domain measurements of HRV predicted mortality and total events. The most powerful predictors was the standard deviation of the means of the 5 min R-R intervals (SDANN index) which was significantly (p < 0.001) lower in Group I than Group II (55 +/- 18 versus 87 +/- 29).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Changes in pulmonary hemodynamics predict benefits in exercise capacity after ACE inhibition in patients with mild to moderate congestive heart failure.

Several causes may affect the efficacy of angiotensin-converting enzyme (ACE) inhibitors in congestive heart failure (CHF). The present study was undertaken to identify what factors might predict benefits in exercise capacity after ACE inhibition in 22 patients with mild to moderate CHF. All patients underwent hemodynamic evaluation before and following an oral dose of quinapril (20 mg). They were then treated daily with 20 mg of quinapril and underwent exercise stress test off-drugs 1 day and 6 months later. Patients were grouped according to their relative changes in vascular resistances after quinapril: Group A (n = 15) showed a greater decrease in pulmonary vascular resistance (PVR) than in systemic vascular resistance (SVR) (% delta PVR/% delta SVR > 1). The opposite occurred in Group B (n = 7). Comparison of pretreatment baseline features revealed that the two groups had similar biochemical and hormonal variables, cardiac index, and SVR. Conversely, Group A patients had higher (p < 0.05) pulmonary artery pressure and PVR compared with Group B patients. Following quinapril, Group A patients showed a greater (p < 0.05) increase in cardiac index than Group B patients, despite a similar reduction in SVR. Accordingly, 1-day drug treatment significantly (p < 0.001) increased exercise duration in Group A (+29%), but not in Group B patients (+7%). Benefits in exercise capacity were still significant (p < 0.001) 6 months later.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1993

Vasotonic angina: a spectrum of ischemic syndromes involving functional abnormalities of the epicardial and microvascular coronary circulation.

OBJECTIVES: The present study was undertaken to investigate the response of large and small coronary arteries in a subgroup of patients with no or minimal coronary artery disease found to have objective signs of myocardial ischemia. BACKGROUND: Many patients apparently have normal coronary arteries despite abnormal electrocardiographic (ECG) changes during spontaneous anginal attacks or exercise stress testing. METHODS: Twenty-five patients with no or minimal (< 30% stenosis) coronary artery disease were chosen from a pool initially selected on the basis of spontaneous anginal attacks and ST segment shifts in the anterior leads. Of these, 10 were grouped as having variant angina (at least one episode of ST elevation) and the remaining 15 as having syndrome X (exercise-induced anginal pain, ST depression and reversible thallium abnormalities). Data were compared with those obtained in 10 patients with stable angina and documented coronary artery disease. Eighteen patients with supraventricular arrhythmias and normal coronary arteries served as control patients. Patients showing focal spasm during ergonovine testing were not included in the subsequent angiographic analysis. Great cardiac vein blood flow, aortic pressure and changes in coronary artery diameter were measured at rest and 2 to 4 min after hyperventilation in the remaining study group. The same procedure was repeated after sublingual administration of 0.3 mg of nitroglycerin in eight patients (four with syndrome X and four with variant angina). RESULTS: Hyperventilation induced diffuse epicardial coronary diameter reduction, which was marginal in control patients (9 +/- 4%) and those with coronary artery disease (5 +/- 3%) but severe (p < 0.001) in those with variant angina (28 +/- 14%) or syndrome X (25 +/- 13%). Concomitant determination of coronary blood flow showed significant (p < 0.001) decreases in those with variant angina (25 +/- 11%) and syndrome X (28 +/- 10%) but not in control patients (5 +/- 8%) or those with coronary artery disease (4 +/- 5%). Changes in great cardiac vein blood flow during hyperventilation were similar before and after nitroglycerin. CONCLUSIONS: These findings indicate that vasoconstrictor stimuli may trigger a diffuse abnormal response of both epicardial and resistance vessels in some patients with chest pain and angiographically normal coronary arteries. Patients showing such diffuse vasoconstrictor abnormalities are suggested to have a single pathogenetic entity with a spectrum of ECG manifestations ranging from ST depression to ST elevation.

Adult↗
PubMed1993

[The development of tolerance to continuous transdermal nitroglycerin therapy in patients with angina of effort and mixed angina].

The present multicentre study, conducted in patients with angina pectoris on chronic therapy with continuous 24-hour transdermal nitroglycerin was aimed at investigating: (1) the actual incidence of nitrate tolerance; (2) the clinical features that characterize those who do not develop tolerance; (3) whether the evidence of clinical and ergometer benefits at 1-month assessment predicts their long-term maintenance. Eligible patients (n = 110; average age 56 +/- 5 yrs) had stable angina pectoris (78 effort angina, 32 mixed angina) with symptom-limited, reproducible cycloergometer tests and were responsive to s.l. nitroglycerin. After a 7-day washout period and a placebo run-in week, all patients were assigned to continuous 10 mg/24-hour nitroglycerin patches (T0). Exercise tests were performed again after 1 month (T1) and 6 months (T6) of treatment. At T1, ergometric data in each patient were compared with those at T0 and showed an increase (> or = 15%) in exercise tolerance in only 61/110 patients: 38 (49%; Group A) of the 78 patients with effort angina and 23 (72%; Group B) of the 32 patients with mixed angina (p < 0.05). Those patients with no significant change in exercise tolerance were assigned to conventional antianginal therapy and were excluded from the study. At T6, both group A and B patients maintained the favourable effects on total exercise duration, time and maximum workload at ischemic threshold and maximal ST depression recorded at T1 vs T0. The weekly attacks of angina and nitroglycerin s.I. consumption decreased significantly in both Group A and Group B patients from the beginning of therapy and throughout the study. These results show that: 1) tolerance to continuous 24-hour transdermal nitroglycerin therapy is not constant phenomenon, but occurs only in a subgroup of patients; 2) patients with mixed angina are more resistant to develop tolerance than those patients with effort angina; 3) the 1-month evidence of clinical and ergometric benefits predicts their maintenance during long-term treatment, as well. These results allow one to hypothesize that the loss of nitrate efficacy on venous pooling capability, but not on arterial tone, might constitute the more frequent cause of tolerance.

Administration, Cutaneous↗
PubMed1992

Coronary hemodynamic effects of systemic thrombolysis in patients with unstable angina.

Intracoronary (i.c.) thrombus is a frequent finding in patients with unstable angina (UA). Accordingly, thrombolytic treatment could be beneficial, as resolution of thrombus might result in increased delivery of blood flow to the ischemic regions. To test this hypothesis, we studied 13 patients with active UA and ST-segment shift in the anterior leads. Coronary angiography was performed and great cardiac vein blood flow (GCVF; thermodilution) was measured in all patients 25 +/- 14 h after the last chest pain episode. Following angiography, patients received i.v. urokinase (UK: 1,000,000 IU/30 min); aortic pressure and GCVF were measured before and every 10 min following drug infusion, for a total time of 90 min. At baseline angiography, 5 of 13 patients (Group 1) had evidence of i.c. thrombus (intraluminal filling defect or thrombotic subocclusion) in the ischemia-related left coronary artery, whereas 8 patients (Group 2) did not. Group analysis showed that UK increased GCVF and decreased anterior coronary resistance in Group 1 (respectively, from 86 +/- 33 to 114 +/- 41 ml/min: p less than 0.005; and from 1.37 +/- 0.68 to 1.01 +/- 0.44 mmHg/ml/min: p less than 0.05) but not in Group 2 (both: p = NS). In conclusion, UK has been shown to increase regional coronary blood flow in selected patients presenting with active UA, as well as evidence of i.c. thrombus at early angiography. Heterogeneity of angiographic findings could explain controversies in trials dealing with thrombolysis in UA.

Aged↗
PubMed1992

Transient ischaemia refractory to conventional medical treatment in unstable angina: angiographic correlates and prognostic implications.

Complex stenosis morphology is frequently seen in patients with unstable angina. However, its relation to transient myocardial ischaemia and clinical outcome has not been adequately elucidated. We studied 86 patients admitted to the Coronary Care Unit for unstable angina; all patients underwent ECG Holter monitoring during the first 2-4 days, while receiving intensive triple drug treatment. Coronary angiography and subsequent analysis of the ischaemia-related artery were performed within 12 days of admission. Patients were grouped according to their angiographic features: 45 showed complex coronary morphology (CM: 29 eccentric stenosis with irregular borders or overhanging edges; 16 intracoronary thrombus), 11 had documented coronary spasm as well as moderate atherosclerosis (CS), seven had left main coronary artery disease, and the remaining 23 patients showed regular and smooth morphology of coronary stenosis (RM). At admission, transient myocardial ischaemia (TMI) was greater in patients with CM (85 +/- 60 min .24 h-1) than in those with RM or CS (33 +/- 26 min .24 h-1; P less than 0.005). After 3 days of full medical treatment TMI decreased in all groups, but 34/45 patients with CM and 9/34 with RM or CS still showed residual ischaemia (greater than 0 min .24 h-1): 76% vs 26%, P less than 0.02. Follow-up was obtained at hospital discharge and after 1 year in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[The relationship between anomalies in the autonomous nervous system and left ventricular dysfunction in patients with hypertrophic cardiomyopathy].

This study was undertaken to assess autonomic nervous system (ANS) activity and its relation to left ventricular function in 40 patients (mean age: 41 +/- 17 years) with hypertrophic cardiomyopathy (HC), in sinus rhythm, off-drugs. Patients were grouped according to the results of radionuclide angiography: 26 had an ejection fraction > 50% (Group A), whereas 14 had an ejection fraction < or = 50% (Group B). Evaluation of parasympathetic activity showed abnormalities in: heart rate (HR) response during Valsalva (< or = 1.1) in 2 Group A (8%) and 12 Group B (86%) patients (p < 0.001); HR variability during deep breathing (< or = 10 b/min) in 2 Group A (8%) and 14 Group B (100%) patients (p < 0.001); immediate HR response to standing (30:15 < or = 1.0) in 2 Group A (8%) and 6 Group B (43%) patients (p < 0.025). Assessment of sympathetic activity showed abnormalities in: systolic blood pressure fall to standing (> 20 mmHg) in 2 Group B (14%) patients only (NS); diastolic blood pressure response to handgrip (< 10 mmHg) in 4 Group B (29%) patients only (p < 0.025). Thus, in HC: impaired parasympathetic control is common in those patients showing left ventricular dysfunction; concurrent sympathetic abnormality may also occur in this subgroup of patients; ANS dysfunction seems to be merely an epiphenomenon which marks the severity of left ventricular derangement.

Adult↗
PubMed1992

[Regional coronary blood flow in patients with acute myocardial infarct treated by systemic fibrinolysis].

Thrombolysis has been reported to restore coronary blood flow in patients with acute myocardial infarction (AMI). However, the relationship between fibrinolytic treatment and evidence of myocardial reperfusion has not been adequately assessed. Accordingly, we measured great cardiac vein blood flow (GCVF:thermodilution) in 12 patients (Group 1) presenting with AMI (chest pain < 4 hours and ST elevation in the anterior leads) before and following i.v. urokinase (UK:2 million U/90 min). Ten patients receiving conventional treatment served as controls (Group 2). UK induced a significant increase of GCVF (from 101 +/- 24 to 164 +/- 42 ml/min, p < 0.001). Maximal increase occurred after 50 +/- 54 min from drug infusion. Conversely, changes in GCVF were not significant in Group 2 (from 103 +/- 35 to 106 +/- 31 ml/min, NS). Following 24 hours changes in GCVF were still consistent only in Group 1 patients. Individual analysis during 24 hours showed marked fluctuations of GCVF peak values in Group 1 patients (62 +/- 43%), but not in Group 2 (29 +/- 21%). Thus, UK induces a marked increase of GCVF in most patients with anterior AMI; such increase suggests that reperfusion occurs early (i.e. within 1 hour) from UK administration. Fluctuations of GCVF during monitoring are magnified by thrombolysis, suggesting intermittent coronary reocclusion in the early hours of AMI.

Blood Flow Velocity↗
PubMed1992

[The differentiated effects of fibrinolysis on the coronary flow in patients with unstable angina].

BACKGROUND: Intracoronary (i.c.) thrombus is a frequent finding in patients (pts) with unstable angina (UA). Accordingly, thrombolytic treatment could be beneficial, as resolution of thrombus might result in increased delivery of blood flow to the ischemic regions. METHODS: To test this hypothesis we studied 13 pts with UA refractory to maximal medical treatment and ST segment shift in the anterior leads. Coronary angiography was performed and great cardiac vein blood flow (GCVF; thermodilution) was measured in all pts within 48 hours (mean 29 +/- 13 hrs) from the last chest pain episode. Following angiography, pts received i.v. wrokinase (UK: 1 million IU/30 min); aortic pressure and GCVF were measured before and every 10 min during drug infusion, for a total time of 90 min. RESULTS: At baseline angiography 5/13 pts (Group 1) had evidence of i.c. thrombus (intraluminal filling defect or thrombotic subocclusion) in the ischemia-related left coronary artery, whereas 8 pts (Group 2) did not. Overall, coronary hemodynamics did not change significantly following drug administration: GCVF was 103 +/- 65 on baseline and 117 +/- 68 ml. min after UK; p > 0.05. Conversely, group analysis showed that UK increased GCVF and decreased anterior coronary resistances (mean aortic pressure/GCVF) in Group 1 (respectively from 86 +/- 33 to 114 +/- 41 ml. min: p < 0.005; and from 1.37 +/- 0.68 to 1.01 +/- 0.44 mmHg/ml. min: p < 0.05) but not in Group 2 (both: p > 0.05), despite similar effects on aortic pressure. CONCLUSIONS: Fibrinolytic treatment can be of therapeutic value in UA; UK has shown to increase regional coronary blood flow in selected pts presenting with refractory angina as well as evidence of i.c. thrombus at early angiography. Heterogeneity of angiographic findings could explain controversies in trials dealing with thrombolysis in UA.

Aged↗