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Biomedical subjects

D R Wallbridge

Publications and source records attributed to D R Wallbridge.

16 recordsLinked to original sources
PubMed1997

Non-invasive assessment of cardiac physiology by tissue Doppler echocardiography. A comparison with invasive haemodynamics.

BACKGROUND: Tissue Doppler echocardiography reveals characteristic patterns of myocardial velocities within systole and diastole which are not well understood. AIM: The purpose of this study was to determine the relationship of myocardial velocity patterns, as assessed by tissue Doppler echocardiography, to the contraction and relaxation phases of the cardiac cycle, as determined during cardiac catheterization. METHODS: Recordings of left ventricular/aortic and left ventricular/pulmonary wedge pressures were obtained simultaneously with apical tissue Doppler echocardiographic images of the left ventricle. A total of 210 cardiac cycles from 22 patients (mean age 58 years, 18 male) undergoing cardiac catheterization were analysed. The time intervals of the different phases of the cardiac cycle were measured from the pressure tracings. These time intervals were correlated to the interfaces of colour myocardial velocity patterns obtained by M-mode tissue Doppler echocardiography. RESULTS: There was a good correlation between the time intervals assessed haemodynamically and those based on the different velocity interfaces obtained with M-mode tissue Doppler echocardiography. Comparable time intervals (from the R wave) obtained by pressure recordings and tissue Doppler echocardiography were, respectively: isovolumic contraction (70 +/- 14 vs 67 +/- 9 ms, r = 0.79); rapid ejection (206 +/- 54 vs 202 +/- 49 ms; r = 0.95); late ejection (357 +/- 36 vs 346 +/- 42 ms. r = 0.93); isovolumic relaxation (405 +/- 43 vs 409 +/- 56 ms; r = 0.95); rapid filling (514 +/- 67 vs 523 +/- 64 ms, r = 0.91); diastasis (697 +/- 153 vs 709 +/- 146 ms, r = 0.98); atrial contraction (890 +/- 128 vs 899 +/- 132 ms, r = 0.96). CONCLUSION: Tissue Doppler echocardiography has the potential to accurately measure the different phases of the cardiac cycle which until now could only be determined invasively. It may provide a sensitive method for the assessment of changes in both cardiac contraction and relaxation in different clinical settings.

Atrial Fibrillation↗
PubMed1996

No attenuation of ischaemic preconditioning by the calcium antagonist nisoldipine.

In anaesthetized dogs, intracoronary infusion of calcium prior to a prolonged ischaemic period reduced infarct size, thereby mimicking the protective effects of ischaemic preconditioning and suggesting that an increase in the intracellular calcium concentration might be an important mechanism underlying this phenomenon. The aim was to determine whether pretreatment with the calcium antagonist nisoldipine attenuates the reduction in infarct size achieved by ischaemic preconditioning. In 10 enflurane-anaesthetized pigs serving as controls (group 1), the inflow into the cannulated left anterior descending coronary artery was reduced (low-flow ischaemia) to achieve a 90% reduction in an anterior myocardial work index (sonomicrometry) for 90 min. In 11 pigs (group 2), a cycle of 10 min of low-flow ischaemia and 15 min of reperfusion (preconditioning) preceded the prolonged ischaemia. In groups 3 (n = 9) and 4 (n = 7), nisoldipine was administered by intravenous infusion (500 ng/kg/min) starting 40 min prior to and then throughout a protocol identical to that of groups 1 and 2, respectively. Subendocardial blood flow was measured with radiolabelled microspheres. Infarct size (% area at risk) was determined by triphenyltetrazolium staining in all pigs after 120 min of reperfusion. Subendocardial blood flow in the area at risk was similar in all four groups (group 1: 0.09 +/- 0.04 ml/min/g; group 2: 0.05 +/- 0.03; group 3: 0.09 +/- 0.03; group 4: 0.07 +/- 0.03). Group 2 had reduced infarct size when compared with group 1 (2.6 +/- 3.0% v 12.4 +/- 8.7%, P = 0.004), and there was a trend for a reduction in infarct size following nisoldipine treatment (group 3: 10.2 +/- 7.1%, group 4: 1.6 +/- 2.8%, P = 0.01). Thus administration of nisoldipine in pigs tended to decrease infarct size, and did not abolish the cardioprotection afforded by ischaemic preconditioning.

Analysis of Variance↗
PubMed1996

Role of endogenous opioids and catecholamines in vasovagal syncope.

Head-up tilt testing demonstrates vasovagal mechanisms as a cause for syncope, but the pathophysiology underlying this condition remains unclear. The aim of this study was (i) to measure plasma beta-endorphins, adrenocorticotrophic hormone, cortisol, catecholamines, and brain natriuretic peptide during head-up tilt, and (ii) to assess the effect of naloxone infusion during head-up tilt in subjects with reproducible vasovagal syncope. During the assessment of unexplained syncope, 71 subjects underwent a total of 93 tilt tests (60-70 degrees head upwards for 40-45 min or until syncope occurred) during which frequent blood sampling was performed. Subjects with a positive tilt test (n = 56) (mean duration to syncope 23.6 min) showed a larger rise in beta-endorphin levels prior to syncope (baseline 4.7 +/- 2.2 vs syncope onset 6.9 +/- 3.2 pmol.l-1, P = 0.0001) than those with a negative test (n = 37) (baseline 3.9 +/- 3.9 vs end of test 4.9 +/- 2.3 pmol.l-1, P = 0.03). During tilting, adrenocorticotrophic hormone, cortisol, and noradrenaline increased; adrenaline and brain natriuretic peptide remained unchanged; and these responses were similar in positive and negative test groups. Naloxone (2.6 mg.kg-1 i.v. bolus followed by 20 micrograms.kg-1.min-1 infusion), administered in a double-blind fashion during head-up tilt in nine subjects, failed to modify either the time to syncope or the vasodepressor response. Thus, endogenous opioids appear not to be an important trigger for vasovagal syncope, and other pathophysiological mechanisms should be considered.

Adrenocorticotropic Hormone↗
PubMed1996

Coronary haemodynamics in left ventricular hypertrophy.

BACKGROUND: Left ventricular hypertrophy is associated with an increased risk of cardiovascular morbidity and mortality. Previous studies have shown that patients with left ventricular hypertrophy develop electrocardiographic changes and left ventricular dysfunction during acute hypotension, and suggest that the lower end of autoregulation may be shifted upwards. AIM: To measure coronary blood flow (velocity) and flow reserve during acute hypotension in patients with left ventricular hypertrophy. PATIENTS: Eight patients with atypical chest pain and seven with hypertensive left ventricular hypertrophy; all with angiographically normal epicardial vessels. SETTING: Tertiary referral centre. METHODS: The physiological range of blood pressure was determined by previous ambulatory monitoring. Left ventricular mass was determined by echocardiography. At cardiac catheterisation, left coronary blood flow velocity was measured using a Judkins style Doppler tipped catheter. During acute hypotension with sodium nitroprusside, coronary blood flow velocity was recorded at rest and during maximal hyperaemia induced by intracoronary injection of adenosine. Quantitative coronary angiography was performed manually. RESULTS: For both groups coronary blood flow velocity remained relatively constant over a range of physiological diastolic blood pressures and showed a steep relation with diastolic blood pressure during maximal hyperaemia with intracoronary adenosine. Absolute coronary blood flow (calculated from quantitative angiographic data), standardised for left ventricular mass, showed reduced flow in the hypertensive group at rest and during maximal vasodilatation. CONCLUSION: The results are consistent with an inadequate blood supply to the hypertrophied heart, but no upward shift of the lower end of the autoregulatory range was observed.

Adenosine↗
PubMed1995

Heart rate variability in left ventricular hypertrophy.

BACKGROUND: Electrocardiographic left ventricular hypertrophy and strain are associated with increased cardiac morbidity and mortality. Impaired cardiac autonomic function, assessed non-invasively by spontaneous heart rate variability on Holter monitoring, is associated with an increased risk of sudden death after myocardial infarction. AIM: To study the effect of left ventricular hypertrophy on heart rate variability. PATIENTS: 36 controls and 154 patients with left ventricular hypertrophy (94 with hypertension and 60 with aortic valve disease). SETTING: Tertiary referral centre. METHODS: Heart rate variability was measured on 24 h Holter recordings by non-spectral methods. Left ventricular mass index and fractional shortening were measured by echocardiography. RESULTS: Patients with left ventricular hypertrophy had a higher left ventricular mass index (P < 0.001) and reduced heart rate variability (P < 0.001) compared with those of the controls. A continuous inverse relation was apparent between heart rate variability and left ventricular mass index (r = -0.478, P < 0.001). Heart rate variability was not affected by age, the presence of coronary artery disease in patients with left ventricular hypertrophy, or beta blocker treatment for hypertension. Multivariate analysis showed that left ventricular mass index is the most important determinant of heart rate variability. CONCLUSION: Heart rate variability is significantly reduced in patients with left ventricular hypertrophy secondary to hypertension or aortic valve disease. A continuous inverse relation exists between heart rate variability and left ventricular mass index. Impaired cardiac autonomic function in left ventricular hypertrophy may contribute to the mechanism of sudden death.

Aortic Valve Stenosis↗
PubMed1995

Intraischemic preconditioning. Increased tolerance to sustained low-flow ischemia by a brief episode of no-flow ischemia without intermittent reperfusion.

Ischemic preconditioning (IP) and myocardial hibernation (MH) are both adaptive phenomena during acute myocardial ischemia, characterized by preserved myocardial viability and attenuated alterations of energy metabolism. Recent data from isolated buffer-perfused rabbit hearts pointed to a further link between IP and MH, in that an initial stimulus of no-flow ischemia was required to permit the development of MH during subsequent sustained low-flow ischemia. In the present study, we therefore investigated in the in situ pig heart whether a brief episode of no-flow ischemia enhances the myocardial tolerance to subsequent sustained low-flow ischemia. By blocking ATP-dependent potassium channels, we attempted to further determine whether such increased tolerance to ischemia is related to IP or MH, since blockade of ATP-dependent potassium channels abolishes the cardioprotection achieved by IP but not by MH. In 8 enflurane-anesthetized pigs serving as controls (group 1), the inflow into the cannulated left anterior descending coronary artery was reduced to achieve a 90% reduction in the anterior myocardial work index (sonomicrometry) for 90 minutes. In 15 pigs (group 2), a 10-minute no-flow ischemic episode preceded 80 minutes of sustained ischemia at a blood flow reduction identical to that in pigs of group 1. In 8 additional pigs (group 3), glibenclamide was administered before the 10-minute no-flow ischemic episode. In all pigs after 120 minutes of reperfusion, infarct size (IS, percentage of area at risk) was determined by triphenyltetrazolium chloride staining. In group 2, IS was reduced (6.8 +/- 6.0% [mean +/- SD], P < .05) when compared with groups 1 (13.2 +/- 9.8%) and 3 (16.7 +/- 8.3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1994

Increase in plasma beta endorphins precedes vasodepressor syncope.

BACKGROUND: Endogenous opioids have a tonic inhibitory effect on sympathetic tone and have been implicated in the pathophysiology of vasodepressor syncope. Plasma beta endorphin concentrations increase after vasodepressor syncope induced by exercise or by fasting. AIMS: To take frequent samples for plasma beta endorphin estimation during tilt testing, and to determine whether plasma beta endorphin increased before the start of syncope. PATIENTS: 24 patients undergoing tilt testing for investigation of unexplained syncope. SETTING: Tertiary referral centre. METHODS: Blood samples were obtained during 70 degrees head up tilt testing. Plasma beta endorphin concentrations were estimated by radioimmunoassay (mean(SD) pmol/l). RESULTS: Patients with a positive test showed a rise in beta endorphin concentrations before syncope baseline 4.4(1.5) v start of syncope 8.5(3.1), p < 0.002). In contrast, patients with a negative test showed no change in beta endorphin concentrations (baseline 3.4(1.0) v end of test 4.5(2.3), NS). After syncope all patients showed a large secondary increase in beta endorphins (32.3(18.6)). CONCLUSION: An increase in plasma beta endorphins precedes vasodepressor syncope. This finding supports a pathophysiological role for endogenous opioids.

Adolescent↗
PubMed1994

Increase in plasma beta endorphins precedes vasodepressor syncope.

BACKGROUND: Endogenous opioids have a tonic inhibitory effect on sympathetic tone and have been implicated in the pathophysiology of vasodepressor syncope. Plasma beta endorphin concentrations increase after vasodepressor syncope induced by exercise or by fasting. AIMS: To take frequent samples for plasma beta endorphin estimation during tilt testing, and to determine whether plasma beta endorphin increased before the start of syncope. PATIENTS: 24 patients undergoing tilt testing for investigation of unexplained syncope. SETTING: Tertiary referral centre. METHODS: Blood samples were obtained during 70 degrees head up tilt testing. Plasma beta endorphin concentrations were estimated by radioimmunoassay (mean(SD) pmol/l). RESULTS: Patients with a positive test showed a rise in beta endorphin concentrations before syncope (baseline 4.4(1.5) v start of syncope 8.5(3.1), p < 0.002). In contrast, patients with a negative test showed no change in beta endorphin concentrations (baseline 3.4(1.0) v end of test 4.5(2.3), NS). After syncope all patients showed a large secondary increase in beta endorphins (32.3(18.6)). CONCLUSION: An increase in plasma beta endorphins precedes vasodepressor syncope. This finding supports a pathophysiological role for endogenous opioids.

Adolescent↗
PubMed1993

A comparison of dobutamine and maximal exercise as stress for thallium scintigraphy.

In the assessment and evaluation of patients with suspected coronary artery disease there is a need for pharmacological stress combined with thallium scintigraphy. Thallium images were obtained following stress both with dobutamine infusion (5-20 micrograms kg-1 min-1) and with symptom-limited bicycle ergometry in 20 patients (age 39-70 years) with chest pain who had been admitted for coronary angiography. Percentage thallium uptake was calculated using a region of interest technique. Detailed comparison was performed of the presence, size and distribution of left ventricular thallium perfusion defects; the percentage thallium uptake in ventricles, lung and liver; and the haemodynamic response to stress. Each stress produced a similar number of abnormal segments in each of three views (total EX 166/300; DOB 167/295), but exercise produced larger defects in the anterior view (P < 0.025). Thallium uptake in left and right ventricles and relative uptake to lungs were similar, but dobutamine produced higher relative liver uptake [EX 1.55 (0.67); DOB 2.97 (1.23) P < 0.0001]. Fourteen patients were able to tolerate dobutamine 20 micrograms kg-1 min-1. The ratio of peak stress to rest double product was smaller with dobutamine in both patients with (DOB 1.3; EX 2.0; P < 0.0047) and patients without beta-blockade (DOB 1.5; EX 2.4; P < 0.008). Dobutamine produced fewer conventional stress endpoints of chest pain and ST depression. In conclusion, dobutamine produces a well-tolerated incremental pharmacological stress with thallium images similar to maximal exercise, and provides a useful alternative stress in patients unable to perform adequate dynamic exercise.

Coronary Angiography↗
PubMedDate not supplied

The potential impact of patient self-referral on mortality in acute myocardial infarction.

Audit is now an important component of the provision of acute cardiology services. In particular, the desire to administer thrombolytic treatment early in acute myocardial infarction has led to a reappraisal of admission procedures. Using records collected prospectively onto a computerized coronary care database for 36 months to December 1991, median delay before arrival at the emergency department and delay between admission and thrombolytic treatment was calculated. Of 1993 consecutive admissions to the coronary care unit, 816 patients had an initial diagnosis of myocardial infarction (later confirmed in 89.6 per cent), and 608 (74.5 per cent) of these received thrombolytic treatment. Overall median delay before arrival at hospital was 147 min. Randomization during the ISIS-3 trial significantly prolonged delays after arrival at hospital (64 vs. 50 min; p < 0.007). General practitioner referral delayed arrival at the emergency department (175 vs. 100 min self-referred; p < 0.0001) and was associated with similar hospital delay (54 vs. 55 min self-referred). Older patients ( > 65 years) presented later in the self-referred group (120 vs. 99 min for age < 65 years; p < 0.04), but there was no difference in the GP-referred group. Previous ischaemic heart disease did not predict type of referral. If delays before thrombolytic treatment are to be reduced significantly patients should be encouraged to seek early medical assistance by telephoning for an ambulance. Delays for patients arriving at the hospital following referral by a GP should be reduced by facilities for direct admission to the cardiologist.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗