Publications
145 results found
Sheridan DJ, McAinsh A, O'Gorman DJ, 1993, The coronary circulation in cardiac hypertrophy., J Cardiovasc Pharmacol, Vol: 22 Suppl 6, Pages: S18-S28, ISSN: 0160-2446
Left ventricular hypertrophy is a common and important risk factor for cardiac mortality and morbidity. Cardiac hypertrophy adversely affects coronary perfusion because hypertension, its most frequent cause, is a major risk factor for coronary disease, and because cardiac hypertrophy may be associated with myocardial ischemia even in the absence of atheromatous coronary disease due to disturbances in coronary physiology. Several studies have demonstrated impairment of coronary reserve in human and experimental cardiac hypertrophy. Normal autoregulation of coronary flow may be disturbed in cardiac hypertrophy for many reasons, including (a) increased perfusion pressure in hypertension, (b) increased diastolic and systolic left ventricular pressures, in addition to disturbed coronary physiology. Studies undertake in the presence of maximal coronary vasodilatation indicate an increased minimal coronary vascular resistance in hypertrophied hearts. Because such measurements were determined in the presence of maximal coronary vasodilation, they are likely to indicate a reduced arteriolar lumenal cross-sectional area per unit mass of tissue. Studies of cardiac and coronary morphology support an imbalance in myocardial and coronary growth in cardiac hypertrophy, but further evidence is needed to confirm this. Myocardial contraction impairs coronary flow, and available evidence suggests that this systolic impairment may be greater in hypertrophied myocardium, and that this may be an additional factor in limiting coronary flow in hypertrophy. A further important feature of impaired coronary reserve in cardiac hypertrophy is its distribution. Studies using radiolabeled microspheres indicate that coronary reserve is reduced in endocardial regions to a much greater extent than epicardial regions. Previously, treatment of conditions such as hypertension, which are commonly associated with hypertrophy, have concentrated on correction of the main defect. It is important to bear in
Burton T, Chakrabarty S, Fluck DS, et al., 1992, Effects of cicletanine on haemodynamics, arrhythmias and extent of necrosis during coronary ligation in rabbits., Br J Pharmacol, Vol: 107, Pages: 1135-1139, ISSN: 0007-1188
1. The effects of cicletanine on arrhythmias, haemodynamics and extent of necrosis during myocardial ischaemia were investigated in rabbits subjected to coronary ligation. 2. Cicletanine increased cardiac output prior to coronary occlusion (P < 0.01) but had no other significant haemodynamic effects at this time and did not significantly alter heart rate, blood pressure or cardiac output during 30 min of ischaemia or 30 min of reperfusion. 3. Ventricular fibrillation and mortality were greater in control (65% and 60% respectively) than treated animals (15.4% and 15.4%, P < 0.01). 4. The extent of myocardial necrosis expressed as a percentage of the area at risk was also reduced by cicletanine from 61 +/- 8% in controls to 37 +/- 6% (P < 0.05). 5. These findings indicate that cicletanine attenuates arrhythmias and preserves myocardium in the early phase of ischaemia and this effect appears to be independent of an established antihypertensive action.
Chakrabarty S, Fluck DS, Flores NA, et al., 1992, Effects of the PAF antagonists BN50726 and BN50739 on arrhythmogenesis and extent of necrosis during myocardial ischaemia/reperfusion in rabbits., Br J Pharmacol, Vol: 107, Pages: 705-709, ISSN: 0007-1188
1. The effects of two novel platelet activating factor (PAF) antagonists BN50726 and BN50739 on arrhythmias, haemodynamics and extent of necrosis during myocardial ischaemia and reperfusion were investigated in anaesthetized rabbits subjected to coronary artery ligation. 2. BN50739 reduced heart rate prior to coronary artery occlusion (P < 0.005) but had no other significant haemodynamic effects at this time. BN50739 and BN50726 did not significantly alter heart rate or blood pressure during 30 min of ischaemia or 30 min of reperfusion, compared to control hearts. 3. BN50739 and BN50726 had no effect on the incidence of arrhythmias during ischaemia. BN50726 significantly reduced the incidence of reperfusion ventricular fibrillation compared to controls (0% v 40%, P < 0.05), and improved survival (80% v 39%, P < 0.05). Similar trends were observed with BN50739. 4. BN50726 reduced the extent of necrosis compared to control hearts (18 +/- 2% v 30 +/- 3%, P < 0.01). A similar trend was observed with BN50739. 5. These results demonstrate that PAF antagonism with BN50726 attenuates reperfusion-induced arrhythmias and preserves myocardium in the early phase of ischaemia, independently of haemodynamic effects.
DAVIES RH, PARKER KH, SHERIDAN DJ, 1992, THE EFFECT OF THE VALSALVA MANEUVER ON WAVE INTENSITY IN THE HUMAN AORTA - AN ANALYSIS USING THE METHOD OF CHARACTERISTICS, JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, Vol: 24, Pages: S41-S41, ISSN: 0022-2828
O'Gorman DJ, Thomas P, Turner MA, et al., 1992, Investigation of impaired coronary vasodilator reserve in the guinea pig heart with pressure induced hypertrophy., Eur Heart J, Vol: 13, Pages: 697-703, ISSN: 0195-668X
Impaired coronary reserve and increased minimal coronary resistance have been documented in several animal models of left ventricular hypertrophy. There is controversy whether the increased minimal coronary resistance is due to vascular or extravascular causes. To test the hypothesis that pressure-overloaded left ventricular hypertrophy (LVH) is associated with a vascular defect, studies were performed using isolated buffer-perfused guinea pig hearts taken 72 +/- 6 days post-aortic banding (LVH n = 13) and compared to sham-operated controls (n = 12). The pressure flow relationship was determined over the range 30-70 mmHg. We defined an extravascular compression index as the percentage increase in flow during maximal arteriolar dilation when systolic forces were excluded during prolonged diastole (2 +/- 0.2 s). In LVH, coronary reserve was reduced (141 +/- 5.5% v 231.7 +/- 24.1%) P less than 0.01 and minimal coronary resistance was increased (4.55 +/- 0.44 v 3.70 +/- 0.37 mmHg.ml-1.min-1.g-1) P less than 0.05. The extravascular compression index was increased in LVH (36.8 +/- 1.4 v 30.5 +/- 2.3%) P less than 0.05. Systole caused a greater increase in resistance in the LVH group than in controls (1.73 +/- 0.26 v 0.95 +/- 0.14 mmHg.ml-1.min-1.g-1) P less than 0.05. These data indicate that during diastole there is impaired minimal coronary resistance of vascular origin. Systole impaired flow to a greater extent in hypertrophied hearts, further reducing the coronary reserve.
Turner MA, Thomas P, Sheridan DJ, 1992, An improved method for direct laryngeal intubation in the guineapig., Lab Anim, Vol: 26, Pages: 25-28, ISSN: 0023-6772
A novel method of direct laryngeal intubation in the guineapig, using a modified laryngoscope blade, is described. The method has been used in over 400 animals and has proved suitable for recovery procedures and repeated intubation.
Jones CJH, Parker KH, Hughes R, et al., 1992, Nonlinearity of Human Arterial Pulse-Wave Transmission, Journal of Biomechanical Engineering-Transactions of the Asme, Vol: 114, Pages: 10-14
MCAINSH AM, OHARE D, SHERIDAN DJ, et al., 1992, CONTINUOUS MEASUREMENT OF OXYGEN-TENSION IN THE ISOLATED GUINEA-PIG HEART USING A PURPOSE DESIGNED OXYGEN-ELECTRODE, JOURNAL OF PHYSIOLOGY-LONDON, Vol: 452, Pages: P126-P126, ISSN: 0022-3751
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O'Gorman DJ, Sheridan DJ, 1991, Abnormalities of the coronary circulation associated with left ventricular hypertrophy., Clin Sci (Lond), Vol: 81, Pages: 703-713, ISSN: 0143-5221
Flores NA, Sheridan DJ, 1991, Electrophysiological effects of alpha-adrenoceptor stimulation in perfused and superfused myocardium., J Mol Cell Cardiol, Vol: 23, Pages: 973-985, ISSN: 0022-2828
To investigate possible mechanisms for the differing electrophysiological actions of alpha-adrenoceptor stimulation in superfused myocardium and isolated, perfused hearts, we compared the cellular electrophysiological responses to methoxamine (10(-7), 10(-6) and 10(-5)M) in isolated, buffer-perfused guinea-pig hearts and superfused right ventricular tissue at 32 degrees C and 37 degrees C. During superfusion at 32 degrees C with 10(-7)M methoxamine, action potential duration increased. Similar increases in action potential duration and refractory period were seen with 10(-6) M methoxamine while with 10(-5)M methoxamine action potential duration increased but refractory period was unchanged. At 37 degrees C, no changes occurred with 10(-7)M and 10(-6)M methoxamine, but with 10(-5)M, action potential duration increased. Perfusion of isolated hearts with 10(-7)M and 10(-6)M methoxamine had no effect on action potential duration and refractory period at 32 degrees C, but with 10(-5)M methoxamine, refractory period increased. No changes occurred in the hearts at 37 degrees C. Methoxamine had no effect on maximum upstroke velocity of the action potential, conduction time, QRS width and pacing threshold in the perfused hearts or the superfused ventricular strips. Methoxamine (10(-6)M) also reduced action potential duration and refractory period in hearts made globally ischaemic, confirming previous results. Thus, methoxamine increases action potential duration and refractory period in superfused ventricular tissue (32 degrees C greater than 37 degrees C), has no effect in normally perfused hearts, but during myocardial ischaemia reduces action potential duration and refractory period.
Chakrabarty S, Thomas P, Sheridan DJ, 1991, Contribution of platelets and platelet-activating factor (PAF) to the arrhythmogenic, haemodynamic and necrotic effects of acute myocardial ischaemia., Eur Heart J, Vol: 12, Pages: 583-589, ISSN: 0195-668X
The effects of alterations in platelet activity on arrhythmias, haemodynamics and extent of necrosis during coronary ligation for 30 min were assessed in rabbits. Reduction of platelet counts to less than 1% of control by intravenous injection of platelet antiserum (1 ml kg-1 i.v.) reduced the volume of necrosed tissue from 23 +/- 2% to 15 +/- 1%, P less than 0.01 (expressed as % of total LV) and attenuated the hypotensive effect of ischaemia. Pretreatment with the platelet activating factor (PAF) antagonist BN 52021 also attenuated the hypotension and necrosis caused by coronary ligation 23 +/- 2% vs 14 +/- 1%, P less than 0.01. Pretreatment with the thromboxane antagonist CGS 13080 attenuated the hypotensive response to ischaemia but had only a very small effect on the area of necrosis. Administration of PAF at 10 min following coronary ligation markedly increased the volume of necrosed tissue 36 +/- 2%, P less than 0.01 and caused VF and haemodynamic collapse in 10 out of 12 animals. Pretreatment with platelet antiserum or the PAF antagonist BN 52021 reversed this effect of PAF. Pretreatment with CGS 13080 attenuated the marked hypotensive effect of PAF but failed to reverse its necrotic or arrhythmogenic effects. These findings indicate that platelet activation contributes to the necrosis and hypotension following coronary ligation and that platelet-activating factor may contribute to this. The ameliorating effects of platelet antiserum or BN 52021 support the concept that inhibition of platelet activity may have a useful role in the treatment of acute myocardial infarction.
Chakrabarty S, Thomas P, Sheridan DJ, 1991, Arrhythmias, haemodynamic changes and extent of myocardial damage during coronary ligation in rabbits anaesthetized with halothane, alpha chloralose or pentobarbitone., Int J Cardiol, Vol: 31, Pages: 9-14, ISSN: 0167-5273
We investigated the incidence of ventricular arrhythmias, extent of myocardial infarction and alteration in haemodynamic parameters during 30 minutes of coronary arterial occlusion in rabbits anaesthetized with halothane, alpha chloralose and pentobarbitone. Ventricular tachycardia and fibrillation occurred in 10 of 15 given halothane and in 11 of 15 animals given alpha chloralose while of 15 animals given pentobarbitone, 5 developed tachycardia and 8 had fibrillation. Following ligation, blood pressure promptly fell in each group to 71-76% of control values at 1 minute and remained low throughout the occlusion period. This was most marked in the group receiving halothane which had significantly lower pressures at 30 minutes than those anaesthetized with alpha chloralose or pentobarbitone (P less than 0.01 in each case). Those receiving halothane also recovered less on reperfusion. Heart rate remained stable with pentobarbitone anaesthesia during coronary occlusion and reperfusion, but promptly declined in the first minute of occlusion in the groups given halothane and alpha-chloralose and then remained low throughout occlusion, especially in the group given alpha-chloralose (P less than 0.001 vs pentobarbitone and P less than 0.01 vs halothane). The extent of myocardial damage was measured from nitroblue tetrazolium-stained sections and expressed as a percentage of the zone at risk, which was obtained in five hearts following 90 minutes coronary ligation. Values were 44.0% with pentobarbitone, 54.0% with alpha chloralose (P less than 0.01 vs pentobarbitone) and 62.1% with halothane (P less than 0.001 vs pentobarbitone). Thus, the choice of anaesthetic employed during experimental myocardial ischaemia may have significant effects on the incidence of ventricular tachycardia, haemodynamic changes and extent of necrosis observed.(ABSTRACT TRUNCATED AT 250 WORDS)
Flores NA, Seghatchian MJ, Sheridan DJ, 1991, Platelet-mediated alterations in cardiac cellular electrophysiology., Blood Coagul Fibrinolysis, Vol: 2, Pages: 367-371, ISSN: 0957-5235
Recent clinical and experimental evidence indicates that platelet activation contributes to the arrhythmogenic effects of myocardial ischaemia, but little is known about the electrophysiological effects produced by controlled platelet activation under conditions of normal perfusion and how these might relate to effects during ischaemia. To investigate this, we studied changes in cardiac cellular electrophysiology and arrhythmogenesis during infusion of platelets [10(8)/ml] in isolated, perfused guinea-pig hearts during normal perfusion and global myocardial ischaemia. Hearts were studied in four groups: group A (n = 4) receiving frozen/thawed (activated) platelets; group B (n = 4) receiving normal platelets in the presence of 10(-9) M platelet activating factor (PAF); group C (n = 9) receiving buffer only during normal perfusion and myocardial ischaemia; group D (n = 9) receiving platelets during normal perfusion and myocardial ischaemia. Infusion of platelets (group D) had no effects during normal perfusion, but activated platelets (group A) decreased action potential duration (APD) from 165 +/- 1 ms to 138 +/- 5 ms (mean +/- SE) at 15 min of normal perfusion (P less than 0.02) and produced ventricular fibrillation (VF) in 3/4 at 21 +/- 1 min. Infusion of platelets in the presence of PAF (group B) produced similar reductions of APD during normal perfusion and VF in 2/4. During ischaemia, platelets (group D) increased the incidence of VF (100% vs 56% group C, P less than 0.05) and enhanced the ischaemia-induced reductions in APD (107 +/- 3 ms vs 121 +/- 5 ms (group C) P less than 0.05 at 15 min).(ABSTRACT TRUNCATED AT 250 WORDS)
Flores NA, Sheridan DJ, 1990, Electrophysiological and arrhythmogenic effects of platelet activating factor during normal perfusion, myocardial ischaemia and reperfusion in the guinea-pig., Br J Pharmacol, Vol: 101, Pages: 734-738, ISSN: 0007-1188
1. Platelet activating factor (PAF) is often used to study the effects of platelet activation. While direct myocardial electrophysiological effects of PAF have been described in superfused myocardial tissue, little is known about its actions on the whole heart. 2. The cellular electrophysiological and arrhythmogenic effects of PAF (10(-11)M, 10(-10)M and 10(-9)M) were studied during normal perfusion, global myocardial ischaemia and reperfusion in Langendorff-perfused guinea-pig hearts at 32 degrees C. 3. PAF (10(-9)M) increased the incidence of ventricular fibrillation during ischaemia and reduced action potential duration (APD) during normal perfusion and early myocardial ischaemia (10(-9)M and 10(-10)M). PAF also reduced refractory period (RP) during normal perfusion (10(-9)M) and early ischaemia (10(-9)M and 10(-10)M). PAF prevented recovery of APD (10(-9)M) and RP (10(-9)M and 10(-10)M) during reperfusion. PAF at a concentration of 10(-11)M had no electrophysiological effects. 4. PAF (10(-9)M) increased the QRS width of the electrocardiogram during late ischaemia while 10(-10)M PAF raised pacing threshold during late ischaemia. 5. Perfusion pressure was increased, and developed tension decreased by 10(-9)M PAF. 6. These results demonstrate that PAF has direct myocardial electrophysiological effects in the whole heart which occur during normal perfusion and are capable of augmenting the effects of myocardial ischaemia, but are independent of the presence of platelets.
Thomas P, Dixon MS, Winterton SJ, et al., 1990, Acute haemodynamic effects of cromakalim in patients with angina pectoris., Br J Clin Pharmacol, Vol: 29, Pages: 325-331, ISSN: 0306-5251
1. We studied the acute haemodynamic effects of cromakalim, a vasodilator which activates smooth muscle potassium channels, in 11 patients with ischaemic heart disease undergoing routine cardiac catheterisation. A similar group of six patients given placebo were studied under identical conditions. 2. There were no significant differences in baseline haemodynamic parameters between the two groups. 3. Following intravenous cromakalim (15 micrograms kg-1) cardiac output increased by 30% (P less than 0.05 vs placebo) while systolic arterial pressure decreased by 8% (P less than 0.05), systemic vascular resistance decreased by 29% (P less than 0.01) and pulmonary vascular resistance decreased by 24% (P less than 0.01) at plasma concentrations of the (+)- and (-)-enantiomers of cromakalim of 6.2 +/- 0.5 ng ml-1 and 10.0 +/- 1.0 ng ml-1 respectively. 4. There were no significant differences in diastolic arterial pressure, left ventricular dP/dt and stroke volume between the two groups. Heart rate increased by 11% following cromakalim but this did not achieve significance. 5. These findings confirm that cromakalim acts primarily as an arteriolar vasodilator producing an improvement in cardiac performance. Cromakalim may be of benefit in the treatment of patients with ischaemic heart disease.
Dixon MS, Thomas P, Sheridan DJ, 1990, A randomized double-blind study of bisoprolol versus atenolol in mild to moderate essential hypertension., Eur J Clin Pharmacol, Vol: 38, Pages: 21-24, ISSN: 0031-6970
We have compared the efficacy and pharmacokinetics of bisoprolol, a new cardioselective beta-adrenoceptor antagonist, with atenolol in a randomized double-blind crossover study in 12 patients (mean age 53.5 y) with mild to moderate essential hypertension. After a two week placebo wash-out period without any antihypertensive therapy, the patients were given bisoprolol 10 mg daily or atenolol 50 mg daily, increasing to 20 mg or 100 mg respectively if the sitting diastolic blood pressure did not fall below 90 mm Hg after two weeks of therapy. Crossover occurred after six weeks of active therapy followed by two weeks of placebo wash-out. After 6 weeks of therapy both drugs significantly reduced sitting and standing diastolic blood pressures (bisoprolol by 15% and 16% respectively, atenolol by 11% in both cases). However, while sitting and standing systolic pressures were significantly reduced by bisoprolol (13% and 16% respectively), only standing systolic pressures were significantly reduced by atenolol (11%), and this reduction was significantly less than with bisoprolol (p less than 0.05). Both drugs similarly reduced mean sitting and standing heart rates. There were no significant differences between the single-dose and steady-state kinetics of either bisoprolol or atenolol. The mean plasma elimination half-life (t1/2) increased from 12.9 to 13.2 h during steady state on bisoprolol and from 7.2 to 11.5 h on atenolol. The apparent volume of distribution (Vz) was greater for bisoprolol than for atenolol after single dosing (235 1 vs 146 1) and at steady state (216 1 vs 137 1), but clearances were similar for both drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
Thomas P, Sheridan DJ, 1990, Vascular selectivity of felodipine: clinical experience., J Cardiovasc Pharmacol, Vol: 15 Suppl 4, Pages: S17-S20, ISSN: 0160-2446
Felodipine is a new calcium antagonist with vascular selectivity. It has a high potency in arterial resistance vessels and no apparent action on capacitance vessels. It lacks significant effects on myocardial contractility and cardiac conduction. It is an effective antihypertensive agent and may be safely combined with beta-adrenoceptor blockade. This report outlines work confirming the vascular selectivity of felodipine by examining its clinical effects in hypertension, ischemic heart disease, and congestive heart failure.
FLORES NA, JUHASZ C, SHERIDAN DJ, et al., 1989, AN IBM PC AT-BASED SYSTEM FOR THE ANALYSIS OF CARDIAC ACTION-POTENTIALS IN REAL-TIME, JOURNAL OF PHYSIOLOGY-LONDON, Vol: 418, Pages: P8-P8, ISSN: 0022-3751
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Kennerdy A, Thomas P, Sheridan DJ, 1989, Generalized seizures as the presentation of flecainide toxicity., Eur Heart J, Vol: 10, Pages: 950-954, ISSN: 0195-668X
A 12-year-old girl developed generalized tonic-clonic seizures following ingestion of flecainide 1500 mg (15 tablets). At presentation, the electrocardiogram showed marked prolongation of the JT interval and marked increase in QRS duration. The initial plasma flecainide level was greater than 4 micrograms ml-1. Supportive therapy was instituted and complete recovery occurred within 48 h. The electrocardiogram returned to normal. The management of class 1 antiarrhythmic agent toxicity is briefly outlined and the association of antiarrhythmic drug toxicity with seizures is reviewed.
Thomas P, Dixon MS, Culling W, et al., 1989, Changes in the haemodynamic responses to exercise, posture and nitrates after treatment of congestive heart failure with an arteriolar vasodilator., Clin Sci (Lond), Vol: 77, Pages: 229-236, ISSN: 0143-5221
1. Haemodynamic responses to exercise, posture and nitrates were measured before and after 8 weeks of therapy with an arteriolar smooth muscle specific calcium antagonist, nicardipine, in eight patients with congestive heart failure (New York Heart Association class II or III). 2. The acute haemodynamic effects of intravenous nicardipine before and after 8 weeks of oral therapy confirmed its vasodilating properties, with similar end-points to the initial response after the 8 week period. 3. After 8 weeks of oral therapy all patients improved by one New York Heart Association class and treadmill exercise duration was significantly increased. In contrast, sitting bicycle exercise duration was not prolonged, although, at the same peak workload, changes in cardiac output, stroke volume and systemic vascular resistance were significantly improved after 8 weeks of therapy. 4. Sublingual glyceryl trinitrate predominantly affected pulmonary vascular resistance before and after chronic therapy with nicardipine, although the effects were less marked after 8 weeks. In contrast, the systemic vascular effects of glyceryl trinitrate were significantly increased after 8 weeks of therapy with nicardipine. 5. Increased vasodilator responses to sublingual glyceryl trinitrate and exercise after chronic treatment with nicardipine, in the absence of significant residual vasodilatation at rest, suggests that indirect changes in systemic arterioles may accompany and possibly contribute to the clinical improvement in heart failure.
Flores NA, Sheridan DJ, 1989, Electrophysiological and antiarrhythmic effects of UK 52,046-27 during ischaemia and reperfusion in the guinea-pig heart., Br J Pharmacol, Vol: 96, Pages: 670-674, ISSN: 0007-1188
1. We studied the antiarrhythmic and electrophysiological effects of UK 52,046-27 (10(-8) M and 5 x 10(-8) M), a highly selective alpha 1-adrenoceptor antagonist, during global ischaemia (flow reduced to 10% of control for 30 min) and reperfusion, in isolated, buffer-perfused hearts of guinea-pigs. 2. The compound had few electrophysiological effects during normal perfusion, although action potential amplitude and Vmax were reduced with 10(-8) M (by 9% and 22%) and refractory period was increased with 5 x 10(-8) M (by 13%) compared to control hearts. 3. Perfusion with 5 x 10(-8) M UK 52,046-27 reduced the incidence of ventricular tachycardia during ischaemia from 67% to 25%, and during reperfusion reduced the incidence of ventricular tachycardia (from 83% to 17%) and ventricular fibrillation (from 67% to 8%). 4. The compound prolonged significantly action potential duration and refractory period during ischaemia and reperfusion. Vmax was reduced to a greater extent during reperfusion in the treated hearts, while greater increases in QRS width and stimulation threshold occurred during ischaemia in the treated group. 5. These results confirm that blockade of the alpha 1-adrenoceptor subpopulation during myocardial ischaemia and reperfusion decreases the incidence of arrhythmias and alters cellular electrophysiology during ischaemia and reperfusion.
Thomas P, Sheridan DJ, 1988, Coronary thrombolysis., Q J Med, Vol: 68, Pages: 657-663, ISSN: 0033-5622
WALKER MJA, CURTIS MJ, HEARSE DJ, et al., 1988, THE LAMBETH CONVENTIONS - GUIDELINES FOR THE STUDY OF ARRHYTHMIAS IN ISCHEMIA, INFARCTION, AND REPERFUSION, CARDIOVASCULAR RESEARCH, Vol: 22, Pages: 447-455, ISSN: 0008-6363
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Dixon MS, Thomas P, Sheridan DJ, 1988, Syncope as the presentation of unstable angina., Int J Cardiol, Vol: 19, Pages: 125-129, ISSN: 0167-5273
A 71-year-old woman presented with syncope in association with unstable angina. Coronary angiography and subsequent postmortem findings demonstrated severe coronary arterial disease. The importance of the association of syncope with unstable angina and possible underlying mechanisms are discussed.
Sheridan JV, Thomas P, Sheridan DJ, 1987, Felodipine in ischaemic heart disease., Drugs, Vol: 34 Suppl 3, Pages: 71-78, ISSN: 0012-6667
The effects of felodipine on haemodynamics and exercise capacity have been studied in patients with angina pectoris. In a study of 11 patients undergoing cardiac catheterisation with concomitant beta-blockade, oral felodipine (0.075 mg/kg) increased resting heart rate by 16%. During atrial pacing at 100 beats per minute, felodipine decreased mean systemic arterial pressure by 9.6% and systemic vascular resistance by 30% and increased cardiac index by 30%. There was no significant effect on pulmonary haemodynamics or left ventricular end-diastolic pressure and the isovolumic and ejection phase indices of left ventricular contractility were unchanged. In a randomised double-blind study of 14 patients, felodipine, when added to regular beta-blockade, reduced the frequency of episodes of angina and the amount of glyceryl trinitrate consumed. At a similar plasma concentration to that in the above study, felodipine significantly increased exercise tolerance by 16%, without producing a change in the maximal double product. Resting supine heart rate was increased by 7.3% after felodipine administration; supine systolic and diastolic blood pressures were decreased by 13% and 12%, respectively, and erect systolic and diastolic blood pressures by 14% and 10%, respectively. Only minor adverse effects were reported. Because of its systemic vasodilating properties, felodipine should be a useful adjunct to beta-blockade in patients with angina pectoris.
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