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Biomedical subjects

R A Tio

Publications and source records attributed to R A Tio.

At least 55 records · Page 3Linked to original sources
PubMed1998

Coronary blood flow dynamics during transcutaneous electrical nerve stimulation for stable angina pectoris associated with severe narrowing of one major coronary artery.

To study the effect of transcutaneous electrical nerve stimulation (TENS) on coronary vasomotion, patients with New York Heart Association class III angina pectoris and significant single-vessel left coronary artery disease and who were also scheduled for elective percutaneous transluminal coronary angioplasty, were allocated to a study group (precordial actual TENS, n = 10) and a control group (precordial simulated TENS, n = 5, and TENS on the back, n = 3). Coronary volumetric flow was assessed in the stenotic and nonstenotic coronary artery before and after neurostimulation. The diameter (in millimeters) of the stenotic coronary artery was reduced in the study group after actual TENS (from 2.73 +/- 0.55 by 0.12 +/- 0.11; p = 0.008). In the nonstenotic coronary artery, the diameter increased in the study group (from 2.64 +/- 0.43 by 0.24 +/- 0.15; p = 0.01). In both the stenotic and nonstenotic coronary arteries, no effect was shown on the average peak velocity (centimeters per second) in the study group. The coronary volumetric flow (milliliters per minute) was reduced in the stenotic artery of the study group (from 62 +/- 18 by 8 +/- 7; p = 0.007). In the nonstenotic coronary artery, volumetric flow increased in the study group (from 57 +/- 18 by 11 +/- 10; p = 0.007). In the control group, simulated TENS and TENS on the back had no effect on the diameter of the artery, average peak velocity, or volumetric flow. In addition, in all patients, TENS had no effect on the total volumetric flow of the left coronary artery and hemodynamic variables during the study period. This observation suggests that TENS modulates regional coronary vasomotion in patients with coronary artery disease.

Aged↗
PubMed1998

Prior cytomegalovirus infection does not predict clinical outcome after percutaneous transluminal coronary angioplasty.

BACKGROUND: A direct association between human cytomegalovirus (HCMV) infection and the development of restenosis after coronary angioplasty has been suggested. The aim of this prospective study was to evaluate the value of HCMV serology in predicting the clinical outcome after percutaneous transluminal coronary angioplasty (PTCA). METHODS AND RESULTS: 112 patients undergoing elective PTCA were included in the study. HCMV antibody levels were measured by ELISA. Cardiac events within a follow-up period of 6 months after PTCA were defined as (1) progression or recurrence of anginal complaints and/or a positive exercise test; (2) restenosis that required repeat revascularization. 73% of PTCA patients were seropositive for HCMV. Successful PTCA was achieved in a total of 94 patients, who were followed for 6 months. In 31/94 patients (33%) cardiac events occurred and in 15/94 (16%), this could be related to restenosis. We found no statistically significant difference between seropositive and negative patients with respect to anginal complaints or the need for revascularization. There was no evidence of acute reactivation, since titers of anti-HCMV antibodies did not increase after PTCA. CONCLUSION: This study shows that the clinical outcome after PTCA is not related to the HCMV serostatus of the patient. Therefore, our data do not support the hypothesis that serological markers of HCMV infection are of clinical importance for the assessment of a patient's individual risk after PTCA. This does not preclude a role for local reactivation of HCMV at the site of angioplasty.

Acute Disease↗
PubMed1998

The assessment of autonomic function in patients with systemic amyloidosis: methodological considerations.

Autonomic neuropathy is a well-known and prognostically important feature of systemic amyloidosis. In other conditions, autonomic function is commonly assessed by cardiovascular reflex tests, described by Ewing, but the feasibility of these tests has not been investigated in patients with systemic amyloidosis. We studied autonomic function in amyloidotic patients using cardiovascular tests and assessed their feasibility. Patients with AA, AL and ATTR amyloidosis participated. In all patients, cardiovascular reflex testing (mental arithmetic stress test and head-up tilting, besides the Ewing-tests) was performed. Of the 46 patients included, only 28 patients could perform all 4 Ewing-tests. In particular, patients with AA amyloidosis secondary to rheumatoid arthritis could not perform standing up and the isometric handgrip test. However, when the mental stress test replaced the handgrip test and head-up tilting replaced standing up, in 45 of the 46 patients, autonomic function could be assessed with cardiovascular reflex tests. Half of the patients with AA amyloidosis had signs of autonomic neuropathy--which was more than expected. We propose to replace the isometric handgrip test with the mental arithmetic stress test and standing up with head-up tilting if a patient is not able to perform these tests.

Adolescent↗
PubMed1997

Evidence for differential sympathetic and parasympathetic reinnervation after heart transplantation in humans.

During heart transplantation (HTX) all neural connections are severed. In humans, signs of autonomic reinnervation have been found. In this study non-invasive tests were used to compare signs of sympathetic and parasympathetic reinnervation. Non-invasive autonomic function tests and heart rate variability parameters (HRV; 24 h electrocardiographic registration) were used to investigate signs of reinnervation. 16 HTX patients (14 males) were compared with age-and sex-matched controls. Parasympathetic heart rate changes in HTX compared to controls were attenuated during the diving test, deep breathing, the Valsalva maneuver and standing up but not during carotid sinus massage. Sympathetic heart rate increases were lower during the cold pressor test and mental stress. The blood pressure responses were comparable to the control group, but not during active standing and tilting. This finding suggests an obligatory 'blood pressure' role for the innervated heart in these two tests. All HRV parameters were lower in HTX. One or more normal parasympathetic responses were found in 13 out of 16 patients versus 4 out of 16 with normal sympathetic responses (p < 0.05). Heart rate variations were less in case of a higher donor age, and higher in case of a longer time after HTX. Parasympathetic signs of reinnervation are more common than sympathetic signs of reinnervation. A higher donor age reduces signs of reinnervation. If the sympatho-vagal balance is a prognostic factor in HTX patients as it is in other cardiac diseases these findings are clinically relevant.

Adult↗
PubMed1997

Sequelae of spinal cord stimulation for refractory angina pectoris. Reliability and safety profile of long-term clinical application.

BACKGROUND: Spinal cord stimulation (SCS) is effective in the treatment of severe coronary artery disease (CAD) unresponsive to anti-anginal medication or revascularization procedures. However, there is still concern about its safety. OBJECTIVE: To investigate the reliability, morbidity, and mortality aspects of SCS in patients with refractory angina pectoris by studying the predictors of outcome, defined by efficacy, adverse events and mortality, in patients with CAD and SCS. METHODS: Fifty-seven patients (18 women) treated with SCS, aged 59.8 +/- 7.6 years (mean +/- SD) were studied retrospectively. They had suffered from manifest CAD for 9.4 +/- 4.9 years; 46 of them had experienced a myocardial infarction prior to the implantation; 28 had had a previous percutaneous transluminal coronary angioplasty; and 52 had undergone coronary artery bypass surgery. The mean left ventricular ejection fraction was 51.8 +/- 13.8%. All of the patients were being treated with two or three anti-anginal drugs. RESULTS: During 2042 patient-months follow-up, nine of the 57 patients died (annual mortality rate 6.5%). The percentage of adverse events requiring reprogramming or surgical reintervention was reduced from 83% for 18 patients with the Medtronic ITREL lead to 33% for 39 patients with the ITREL II system. The clinical outcome was correlated positively with a left ventricular ejection fraction > 40% (P = 0.0005), and negatively with a high cholesterol level (P = 0.0042), more prior revascularizations (P = 0.028), and a higher New York Heart Association classification (P = 0.04). CONCLUSIONS: Improvement of the SCS system reduced the equipment-related complication rate. The predictors of outcome are related to the traditional risk factors for CAD. The mortality rate of patients with refractory angina treated with SCS is similar to that of patients with CAD and stable angina pectoris.

Angina Pectoris↗
PubMed1997

Myocardial bridging in a survivor of sudden cardiac near-death: role of intracoronary doppler flow measurements and angiography during dobutamine stress in the clinical evaluation.

Extensive myocardial bridging in the left anterior descending coronary artery was found in a 46 year old survivor of sudden cardiac near-death. Positron emission tomography and dobutamine stress echocardiography revealed ischaemia in the myocardium distal to the bridging. Spasm was excluded as cause of the ischaemia by intracoronary infusion of acetylcholine. Further evaluation of the haemodynamic importance of the bridging using intracoronary Doppler flow velocity measurements revealed an abnormal flow reserve. Dobutamine stress during coronary angiography caused increased mechanical compression during diastole. This was accompanied by multiple premature ventricular contractions. After a debridging operation the flow velocity reserve was normal. The abnormalities found during dobutamine stress had disappeared. Unexpectedly, a spasm was inducible. This may have been due to local oedema or scar formation after the operation. For the evaluation of the haemodynamic importance of myocardial bridging, intracoronary Doppler flow velocity measurements and angiography during dobutamine stress may be helpful in clinical decision making.

Cardiotonic Agents↗
PubMed1994

Coronary artery bypass grafting early after acute myocardial infarction in patients initially treated with thrombolytic therapy or coronary angioplasty.

BACKGROUND: Treatment of patients with acute myocardial infarction should aim to restore blood flow in the infarct-related artery as soon as possible. Thrombolytic therapy has recently been compared with direct angioplasty; however, these interventions may not be sufficient, and coronary artery bypass grafting (CABG) may be necessary. METHODS: In a series of 301 patients with acute myocardial infarction, randomly assigned either to receive intravenous streptokinase (n = 149) or to undergo percutaneous transluminal coronary angioplasty (PTCA; n = 152), 31 patients (aged 61 +/- 10 years; 27 men, four women) underwent CABG within 6 weeks of acute myocardial infarction. RESULTS: Twelve patients (nine in the PTCA group and three in the streptokinase group) underwent surgery within 48 h of the onset of symptoms. Bypass surgery was performed in the streptokinase group on failure of thrombolytic therapy (n = 2), recurrent ischemia (n = 4), or postinfarct angina (n = 9). In the PTCA group, CABG was performed for left main stenosis (n = 6), failed PTCA (n = 3), recurrent ischemia (n = 2), or postinfarct angina (n = 5). An intra-aortic balloon pump (IABP) was required in 15 patients (five streptokinase and 10 PTCA). Major complications after CABG were more common among patients who underwent surgery within 48 h than those after 48 h (eight in 12 patients versus four in 19, respectively). After 17.0 +/- 8.6 months (range 3-33 months), two patients had died; one of end-stage heart failure after 3 months, and one of a stroke after 16 months (both were in the PTCA group and one had undergone surgery within 48 h). One patient suffered a reinfarction after 11 months and one a non-fatal stroke after 1 month (both underwent CABG within 48 h). The left ventricular ejection fraction did not differ between the groups (43 +/- 15% for the 'early' group and 42 +/- 11% for the 'late' group). CONCLUSION: CABG can be performed safely and effectively after initial treatment with direct angioplasty or thrombolytic therapy after acute myocardial infarction. If it is performed within 48 h of onset of symptoms, (in-hospital) morbidity is higher, without affecting mortality or left ventricular function.

Aged↗
PubMed1992

Late potentials in a porcine model of anterior wall myocardial infarction and their relation to inducible ventricular tachycardia.

In this study, normal values for signal averaged electrocardiographic parameters were assessed in healthy pigs (n = 100) and the development of late potentials after myocardial infarction (n = 41) in relation to inducible ventricular tachycardia was investigated. Normal values are: filtered QRS duration (QRS) < or = 78 msec; root mean square voltage of the averaged QRS complex (V(tot)) > or = 51 microV, and duration of terminal activity below 30 microV (D30) < or = 37 msec. The distribution of the root mean square voltage in the last 30 msec (V30) was biphasic. Two weeks after myocardial infarction, QRS was prolonged from 55 +/- 10 to 66 +/- 19 msec (P < 0.002). D30 was prolonged from 19 +/- 6 msec to 28 +/- 13 (P < 0.002). V30 was decreased from 107 +/- 135 microV to 45 +/- 77 (P < 0.02). The total voltage (V(tot)) was decreased from 195 +/- 78 to 123 +/- 61 microV (P < 0.002). In four pigs (19%) late potentials developed. Sustained ventricular tachycardia was inducible in 11 pigs (52%), ventricular fibrillation in two pigs (10%) and eight pigs (38%) were noninducible. Three of 11 inducible pigs and one of the noninducible pigs had a late potential. The incidence of late potentials and their relation to inducible sustained ventricular tachycardia is comparable to the situation in man. Therefore, this pig model is an attractive alternative to the commonly used dog models.

Animals↗
PubMed1992

ACE inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease.

BACKGROUND: In humans, angiotensin converting enzyme (ACE) inhibition attenuates the vasoconstriction induced by sympathetic stimulation in a number of peripheral districts. Whether this is also the case in the coronary circulation is unknown, however. METHODS AND RESULTS: In nine normotensive patients with angiographically assessed coronary atherosclerosis, we measured the changes in mean arterial pressure (intra-arterial catheter), heart rate, rate-pressure product (RPP), coronary sinus blood flow (CBF, thermodilution method), and coronary vascular resistance (CVR, ratio between mean arterial pressure and CBF) induced by the cold pressor test (CPT, 2 minutes) and diving (30 seconds), i.e., two stimuli eliciting a sympathetic coronary vasoconstriction. The measurements were performed in the control condition and 30 minutes after captopril 25 mg p.o. In the control condition, CPT caused an increase in mean arterial pressure and heart rate. Despite the increase in RPP (+20.7 +/- 3.2%, p less than 0.01), CBF did not change and CVR increased (+12.2 +/- 4.0%, p less than 0.05). diving caused an increase in mean arterial pressure and a reduction in heart rate. RPP increased (+14.3 +/- 3.5%, p less than 0.01), but despite this increase, there was a reduction in CBF and a marked increase in CVR (+37.3 +/- 7.4%, p less than 0.01). Captopril did not modify the blood pressure and heart rate responses to both stimuli except for a slight accentuation of the bradycardia to diving. Despite the unchanged or only slightly reduced RPP response, the increase in CVR was markedly and significantly attenuated (p less than 0.01). CONCLUSIONS: ACE inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease. This is probably due to removal of the facilitating influence of angiotensin II on sympathetic modulation of coronary vasomotor tone.

Angiotensin II↗
PubMed1992

Effects of converting enzyme inhibitors on coronary flow and myocardial ischemia.

The regulation of coronary hemodynamics is a complex process. One important factor that interferes with the regulation of coronary tone is the pathophysiological state of the vessels: stimuli that in normal vessels provoke no or only a slight vasoconstriction may cause a severe vasoconstriction in diseased vessels. This effect is related to the function of the endothelium and its ability to produce nitric oxide and prostaglandins. The presence of a local renin-angiotensin system implies the possibility of influencing the coronary flow via interference with this local system. Therefore, it is interesting to determine the effects of converting enzyme inhibitors on coronary flow. In animal experiments, a bradykinin-dependent coronary vasodilation by angiotensin-converting enzyme (ACE) inhibitors is suggested. However, reports on the effect of converting enzyme inhibitors in patients with angina pectoris are not consistent. Some authors found an increase in coronary flow and others found no change or a decrease. The importance of the activation of the renin-angiotensin system is discussed. Moreover, it is shown that captopril reduces sympathetic-mediated coronary vasoconstriction during the cold pressor test and that captopril enhances the parasympathetic-mediated bradycardia during the diving response. In conclusion, the effects of converting enzyme inhibitors on coronary flow is an interesting but not fully understood topic. Therefore, the multifactorial mechanism of action of converting enzyme inhibitors deserves further investigation. There are probably subgroups of anginal patients who may benefit from converting enzyme inhibitor therapy. These subgroups have to be defined. Especially, the finding that a converting enzyme inhibitor reduces sympathetically induced coronary vasoconstriction seems promising.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

Coronary vasodilation induced by captopril and zofenoprilat: evidence for a prostaglandin-independent mechanism.

In this study, the vasodilating properties of captopril and zofenoprilat, two angiotensin-converting enzyme (ACE) inhibitors containing the sulfhydryl group, are investigated in the isolated rat heart. It is demonstrated that both compounds increase coronary flow in a dose-dependent manner. However, the mean pD2 of zofenoprilat appears to be significantly higher than the mean pD2 of captopril (4.55 +/- 0.06 and 3.35 +/- 0.02 respectively), indicating that zofenoprilat is about ten times more potent in increasing coronary flow than captopril. Possibly this difference in potency between captopril and zofenoprilat can be explained by their physicochemical properties. Since zofenoprilat is more lipophilic than captopril, its concentration in cardiac and vascular tissues at distribution equilibrium is thought to be higher than the tissue concentration of captopril, which may result in a more pronounced vasodilatory action. The precise mechanism of coronary vasodilation induced by ACE inhibitors containing the sulfhydryl group is not yet understood. Several factors have been proposed, such as stimulation of prostacyclin production. However, in this study, concomitant administration of 10(-6) mol/l acetylsalicylic acid shows no antagonism, indicating that under normoxic conditions the vasodilatory effects of captopril and zofenoprilat are independent of the production of vasodilating prostaglandins. Therefore, other factors than stimulation of prostacyclin synthesis seem to be involved, such as prevention of bradykinin breakdown and/or potentiation of endothelium derived relaxing factor (EDRF). Furthermore, despite a marked inhibition of prostacyclin production, 10(-6) mol/l acetylsalicylic acid itself has no effect on coronary flow. These results suggest that prostacyclin does not play an important role in the regulation of coronary flow, at least in the normoxic isolated rat heart.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

In vivo effect of bradykinin during ischemia and reperfusion: improved electrical stability two weeks after myocardial infarction in the pig.

In this study, the effect of bradykinin or saline infusion during ischemia and reperfusion on electrical stability, 2 weeks after myocardial infarction, was assessed. Acute myocardial infarction was induced in 21 pigs by a transluminal occlusion of the left coronary artery with a catheter balloon, inflated for 45 min. Bradykinin was administered by a 30-min infusion that started after 30 min of coronary occlusion and was continued until 15 min after reperfusion. Although creatine kinase levels in bradykinin-treated animals were significantly lower (p less than 0.001), 2 week survival was not different between groups. In survivors, the filtered QRS (ventricular deflection) duration (detected using signal-averaged electrocardiography) was significantly prolonged in saline-treated pigs, whereas in bradykinin-treated pigs this prolongation was prevented. The terminal voltage of the QRS complex was significantly lower in saline-treated pigs than in bradykinin-treated pigs. These two parameters signify an improved electrical stability after bradykinin treatment. Refractory periods in saline-treated hearts were longer than in bradykinin-treated hearts (106 +/- 10% vs. 95 +/- 13%, p less than 0.05). Also, current thresholds in the infarct border zones showed a greater variance in saline-treated hearts (p less than 0.001), pointing toward more tissue heterogeneity of the infarct border zone. Programmed electrical stimulation showed a trend toward reduced inducibility of sustained ventricular tachycardia in bradykinin-treated hearts. Therefore, bradykinin improves electrical stability weeks after experimental myocardial infarction.

Animals↗
PubMed1991

Effects of bradykinin on inducible sustained ventricular tachycardia two weeks after myocardial infarction in pigs.

We studied the in vivo effect of bradykinin infusion on inducible sustained ventricular tachycardia (VT) 2 weeks after myocardial infarction in pigs, based on the assumption that the antiarrhythmic effect of angiotensin-converting enzyme (ACE) inhibitors may, apart from their angiotensin-II lowering effect, also be due to elevation of endogenous bradykinin levels. Of the six pigs with inducible VT in the control state, four were noninducible during subsequent bradykinin infusion (p less than 0.05). The ventricular effective refractory period (VERP) did not change during bradykinin infusion (from 237 +/- 37 to 239 +/- 42 ms), nor did intraventricular conduction change (filtered QRS duration was 45 +/- 17 ms before and 43 +/- 19 ms during infusion). Bradykinin caused both a significant systolic blood pressure (SBP) decrease (from 79 +/- 14 to 49 +/- 4 mm Hg, p less than 0.001) and diastolic BP (DBP) decrease (from 41 +/- 10 to 27 +/- 4 mm Hg, p less than 0.01). In conclusion, exogenous bradykinin reduced the inducibility of sustained VT 2 weeks after myocardial infarction. Because refractory periods or conduction velocity were not affected, the mechanism of action might be associated with the BP decrease, which can decrease wall stress. The previously reported antiarrhythmic effect of ACE inhibitors may be due in part to elevation of endogenous bradykinin levels.

Animals↗