A new approach to scoring systems to improve identification of acute medical admissions that will require critical care.

Removal of the intensive care unit (ICU) at the Vale of Leven Hospital mandated the identification and transfer out of those acute medical admissions with a high risk of requiring ICU. The aim of the study was to develop triaging tools that identified such patients and compare them with other scoring systems. The methodology included a retrospective analysis of physiological and arterial gas measurements from 1976 acute medical admissions produced PREEMPT-1 (PRE-critical Emergency Medical Patient Triage). A simpler one for ambulance use (PREAMBLE-1 [PRE-Admission Medical Blue-Light Emergency]) was produced by the addition of peripheral oxygen saturation to a modification of MEWS (Modified Early Warning Score). Prospective application of these tools produced a larger database of 4447 acute admissions from which logistic regression models produced PREEMPT-2 and PREAMBLE-2, which were then compared with the original systems and seven other early warning scoring systems. Results showed that in patients with arterial gases, the area under the receiver operator characteristic curve was significantly higher in PREEMPT-2 (89·1%) and PREAMBLE-2 (84.4%) than all other scoring systems. Similarly, in all patients, it was higher in PREAMBLE-2 (92·4%) than PREAMBLE-1 (88·1%) and the other scoring systems. In conclusion, risk of requiring ICU can be more accurately predicted using PREEMPT-2 and PREAMBLE-2, as described here, than by other early warning scoring systems developed over recent years.

Fish oil before cardiac surgery: neutrophil activation is unaffected but myocardial damage is moderated.

Could pre-operative dietary intervention with fish oil reduce neutrophil activation and myocardial damage associated with cardiopulmonary bypass (CPB)? Patients were randomised to receive either 8 g/day fish oil (n=22) or placebo (n=18) for 6 weeks. Neutrophil activation, apoptosis and cardiac damage were measured. Demographics and operative variables were similar. Fish oil diet decreased plasma VLDL from 0.69+/-0.34 to 0.51+/-0.24 mmol/l and triglycerides from 1.68+/-0.70 to 1.39+/-0.54 mmol/l. HDL cholesterol increased from 0.94+/-0.27 to 1.03+/-0.26 mmol/l demonstrating significant treatment effects (P=0.007, 0.02 and 0.0003, respectively) as well as compliance with treatment. There were no significant differences in ex vivo N-formyl-methionyl-leucyl-phenylalanine-stimulated neutrophil superoxide anion generation or myeloperoxidase release at recruitment, pre-operatively and at end-CPB. Apoptosis at end-CPB was equally reduced in both groups from 23+/-9% to 13+/-4% in the fish oil group (P<0.001) and 35+/-14% to 15+/-3% in the placebo group (P=0.001). At end-CPB overall troponin I levels averaged 0.91+/-0.60 ng/ml which clearly exceeded diagnostic levels (0.15 ng/ml). At 24h troponin I fell significantly in the fish oil group to 46+/-23% of end-CPB levels (P=0.0002) whereas it peaked in the placebo group to 107+/-72% (P=0.098 vs. end-CPB); this difference was significant: P=0.013. At 48 h the placebo-treated patients had higher troponins but not significantly so (P=0.059). Area-under-the-curve analysis did not conclusively support this (P=0.068). We conclude that fish oil did not significantly decrease post-CPB neutrophil activation (as detected ex vivo) but may moderate post-operative myocardial damage.

Dispersion of coronary artery thrombi by antagonism of platelet serotonin receptor in the dog.

OBJECTIVE: Blockade of platelet 5HT2 receptors prevents coronary artery thrombi. This study explores the dispersal of established thrombus by such 5HT2 antagonism. METHODS: Seven open chest anaesthetised beagles were used in a repeated measures study of the action of MDL 11,939 to remove the participation of platelet 5HT2 receptors in the natural history of intracoronary thrombosis with cyclic blood flow reduction. Endothelial damage and critical diameter constrictors were applied to the circumflex coronary artery, and systemic blood pressure and circumflex blood flow were measured continuously. RESULTS: Cyclic flow reductions, which were established by build up and embolisation of platelet thrombi, were completely abolished by the 5HT2 antagonist MDL 11,939. The dose given in the first two experiments was 0.5 mg.kg-1, reduced to 0.2 mg.kg-1 for the third. Subsequent animals received 0.1 mg.kg-1. Mean blood pressure rose slightly. Adrenaline infusion at 0.4 micrograms.kg-1.min-1 failed to restore cyclic flow reductions in any animal and caused a small flow increase without affecting mean blood pressure. The pattern of blood flow restitution after administration of MDL 11,939 was of great interest. In all the animals flow spontaneously increased in a stepwise fashion (a double step in five dogs). The step up was markedly different from the increase in flow seen during adrenaline infusion. CONCLUSIONS: (1) These results are further evidence of the importance of serotonin as a mediator of platelet thrombus in stenosed coronary arteries. (2) The apparent dissipation of thrombi by MDL 11,939 may be of importance.

The pressure-flow relation in the canine coronary artery: combined effects of critical stenosis and intracoronary thrombosis.

OBJECTIVE: To characterise the effect of coronary intra-arterial thrombosis upon the downstream vascular bed. BACKGROUND: The vascular response downstream from a coronary intra-arterial thrombus has not previously been characterised. We postulated that downstream vasoconstriction might result from the presence of endothelial damage with consequent growth of platelet-rich thrombus. METHODS: We measured the pressure gradient and flow across, and the pressure/flow ratio distal to, a canine left circumflex artery stenosis with and without endothelial damage causing intracoronary thrombosis. We also observed the effects of transient complete conclusions. RESULTS: At occlusion, the pressure gradient was maximal; relief of occlusion caused a rapid increase flow and distal pressure with a rapid decrease in stenosis pressure gradient and resistance. Subsequently there was a period of stable stenosis resistance with pressure gradient and flow declining; distal pressure therefore increased at this time. Finally in the thrombus group only, stenosis resistance increased again towards re-occlusion. During occlusion, distal pressure averaged 49 +/- 18 mmHg in the presence of thrombus vs. 22 +/- 4 mmHg in its absence (P < 0.001). Following release of occlusion, the flow increased faster than distal pressure, so that the ratio (distal pressure/flow) fell rapidly. Subsequently, distal pressure continued to increase after flow had reached a peak and begun to decline, suggesting vasoconstriction. In the presence of thrombus, the distal pressure/flow ratio was higher than in the absence of thrombus, both at maximal vasodilation (P < 0.005) and at maximum vasoconstriction (P < 0.025). CONCLUSIONS: During cyclic flow variations the stenosis resistance changes are exactly as expected from thrombus growth and embolisation. The distal pressure/flow ratio showed a time-dependent increase which appeared greater when conditions favoured intracoronary thrombosis.

Downstream resistance effects of intracoronary thrombosis in the stenosed canine coronary artery.

OBJECTIVE: The presence is well established in unstable angina of intracoronary thrombosis in a stenosed epicardial coronary artery. The effects of the thrombus formation on the distal microcirculation are however still unclear. METHODS: We adapted the Folts canine model of left circumflex coronary arterial stenosis and intracoronary thrombosis by the insertion of a pressure catheter distal to the stenosis and by the use of 15 microns radioactive microspheres for measurement of regional myocardial blood flow. This permitted measurement during circumflex artery occlusion of collateral flow, downstream vascular resistance and collateral resistance. RESULTS: Distal circumflex resistance, obtained by dividing the distal circumflex coronary pressure gradient by the collateral flow, significantly increased with thrombosis (94.47 +/- 35.72 to 120.06 +/- 34.47; p = 0.0018) mmHg/ml/min/g. Changes in collateral flow and resistance in the presence of thrombosis, during maximum ischaemic vasodilatation, were inconsistent. CONCLUSION: Thrombosis causes increased vascular resistance in the microcirculation distal to the site of injury. This may be of clinical relevance in unstable angina, characterised by episodes of thrombus growth and embolization, in which ischaemic episodes may be worsened by generalised downstream vascular changes.

Measurement of coronary collateral flow and resistance in the presence of an open critical stenosis, and the response to intra-arterial thrombosis.

OBJECTIVE: (1) Can one measure coronary collateral flow around an open critical stenosis? (2) Does intracoronary platelet thrombosis affect native coronary collateral vessels? METHODS: We measured regional myocardial blood flow by the radioactive microsphere technique in seven anaesthetised dogs with an ultrasonic flowmeter on the circumflex branch of the left coronary artery (LCx). Measurements were made (a) in a control period, (b) after induction of a tight stenosis on the LCx, and (c) after additional arterial damage at the stenosis to induce intraluminal thrombosis. Collateral flow was calculated from LCx tissue flow(in ml/min/g tissue) minus LCx flowmeter flow which is in ml/min. Therefore, it was necessary to use scaling by reference back to the control measurements and conversion to ml/min/g tissue equivalent. RESULTS: LCx stenosis induced collateral flow from the other coronary arteries into the LCx area of supply, which decreased (mean+/-S.E.) from 0.23+/-0.03 to 0.15+/-0.05 ml/min/g tissue with thrombosis. Collateral resistance correspondingly increased with thrombosis from 187.6+/-18. 2 to 1069+/-544 mmHg/ml/min/g (P<0.02). CONCLUSION: Coronary collateral flow around an open stenosis can be measured by reference back to control conditions. The coronary collaterals vasoconstrict in the presence of thrombosis even though they are in the stream of blood coming from normal coronary arteries.

Macroaggregation of platelets in plasma, as distinct from microaggregation in whole blood (and plasma), as determined using optical aggregometry and platelet counting respectively, is specifically impaired following cardiopulmonary bypass in man.

We determined changes in platelet aggregability following cardiopulmonary bypass, using optical aggregometry to assess macroaggregation in platelet-rich plasma (PRP), and platelet counting to assess microaggregation both in whole blood and PRP. Hirudin was used as the anticoagulant to maintain normocalcaemia. Microaggregation (%, median and interquartile range) in blood stirred with collagen (0.6 micrograms/ml) was only marginally impaired following bypass (91 [88, 93] at 10 min postbypass v 95 (92, 96] prebypass; n = 22), whereas macroaggregation (amplitude of response; cm) in PRP stirred with collagen (1.0 micrograms/ml) was markedly impaired (9.5 [8.0, 10.8], n = 41 v 13.4 [12.7, 14.3], n = 10; p < 0.0001). However, in PRP, despite impairment of macroaggregation (9.1 [8.5, 10.1], n = 12), microaggregation was near-maximal (93 [91, 94]), as in whole blood stirred with collagen. In contrast, in aspirin-treated patients (n = 14), both collagen-induced microaggregation in whole blood (49 [47, 52]) and macroaggregation in PRP (5.1 [3.8, 6.6]) were more markedly impaired, compared with control (both p < 0.001). Similarly, in PRP, macroaggregation with ristocetin (1.5 mg/ml) was also impaired following bypass (9.4 [7.2, 10.7], n = 38 v 12.4 [10.0, 13.4]; p < 0.0002, n = 20), but as found with collagen, despite impairment of macroaggregation (7.2 [3.5, 10.9], n = 12), microaggregation was again near-maximal (96 [93, 97]). The response to ristocetin was more markedly impared after bypass in succinylated gelatin (Gelofusine) treated patients (5.6 [2.8, 8.6], n = 17; p < 0.005 v control), whereas the response to collagen was little different (9.3 v 9.5).(ABSTRACT TRUNCATED AT 250 WORDS)

Limitation of infarct size by trimetazidine in the rabbit.

The influence of trimetazidine on infarct size was studied with a 45-minute period of coronary occlusion followed by 24 hours of blood reperfusion in the rabbit heart. The groups studied were 7 control rabbits and 7 rabbits pretreated with 3 mg/kg of trimetazidine. Twenty-four hours after coronary artery ligation for 45 minutes, infarct size was measured in myocardial slices using trinitrophenyl tetrazolium staining, and the area at risk was determined by injection of zinc/cadmium particles and delineated at the same time by imaging, under fluorescent light, the areas of tissue that fluoresced. The range of area at risk was similar in both of the groups. There was a significant reduction in the size of infarct that developed in the trimetazidine-treated group when compared with the control rabbits. It is concluded that pretreatment with trimetazidine in the blood-perfused rabbit heart is effective in reducing myocardial infarct size.

The effects of heparin and extracorporeal circulation on platelet counts and platelet microaggregation during cardiopulmonary bypass.

BACKGROUND: Cardiopulmonary bypass is associated with platelet activation and reduced platelet counts. Platelet activation may artifactually lower platelet counts by causing aggregation. In vivo platelet activation may increase existent platelet microaggregation ex vivo. We studied platelet counts and existent platelet microaggregation at different stages of cardiopulmonary bypass. METHODS: Twenty-one patients were studied before and after heparinization (300 U. kg(-1)) and at the end of cardiopulmonary bypass. Unaggregated (or single) platelets were counted in hirudin-anticoagulated blood, and total platelets were counted in ethylenediaminetetraacetic acid-anticoagulated blood. RESULTS: The total platelet count, 198 +/- 61 x 10(9). L(-1), was unaffected by heparin and stayed at 197 +/- 60 x 10(9). L(-1) (P =.7) but fell during extracorporeal circulation; the hemodilution-corrected count was 163 +/- 52 x 10(9). L(-1) (P =.0004). Heparinization reduced the unaggregated platelet count from (mean +/- 1 SD) 178 +/- 62 x 10(9). L(-1) to 155 +/- 60 x 10(9). L(-1) (P =.0001). Extracorporeal circulation had little additional effect. The hemodilution-corrected count was 142 +/- 48 x 10(9). L(-1) (P =.6). CONCLUSIONS: Heparinization caused platelet activation and increased existent platelet microaggregation ex vivo. During extracorporeal circulation, there was a reduction in total platelets that was greater than could be explained by hemodilution alone, but the unaggregated platelet count did not change significantly when corrected for hemodilution. Furthermore, the increased platelet microaggregation observed after heparinization was no longer evident after this loss. These findings suggest that during extracorporeal circulation, the platelets that formed into microaggregates after heparinization were lost from the circulation in preference to single platelets.

Histologically diagnosed Helicobacter pylori in heart transplant recipients.

BACKGROUND: The role of Helicobacter pylori in the pathogenesis of nonautoimmune gastritis and peptic ulceration is well recognized. H. pylori is widely prevalent in the general population, but the incidence among heart transplant recipients has not been reported. Furthermore, the natural history of this infection may be modified by immunosuppression. METHODS: Gastric and duodenal biopsy specimens from 47 heart transplant recipients were examined over a period of 44 months. RESULTS: Twenty-three (49%) patients had H. pylori infection (15 men, 8 women; mean age 49 [range 35 to 59] years). Eight of the 23 (35%) had symptoms. These eight patients were treated for H. pylori with bismuth, metronidazole, and amoxicillin, followed by maintenance H2-receptor antagonists. Dyspepsia continued in six of these patients, with persistence or recurrence of H. pylori being demonstrated in four. CONCLUSIONS: This study shows that although histologically diagnosed H. pylori infection is widely prevalent among heart transplant recipients, this prevalence is very similar to the general population. Immunosuppression may play a role in the recurrence or persistence of this infection and may diminish the mucosal inflammatory response to the organism.

Marfanoid aneurysm in donor aorta after transplantation.

A case is reported of dissecting aneurysm of the donor ascending aorta and root 4 years after orthotopic cardiac transplantation. The pathology raises the possibility of Marfan's syndrome in the donor.

Heparin-induced platelet dysfunction and cardiopulmonary bypass.

BACKGROUND: Cardiopulmonary bypass is associated with impaired platelet macroaggregation. Heparin contributes to platelet dysfunction before extracorporeal circulation. In vitro heparinization of whole blood does not impair macroaggregation. Heparin releases several endothelial proteins; thus heparin may inhibit macroaggregation indirectly. METHODS: Patients undergoing operations using cardiopulmonary bypass and ABO blood group compatible volunteers were studied. Whole blood impedance aggregometry assessed macroaggregation in response to collagen (0.6 microg ml(-1)) in blood diluted either with normal saline or with platelet poor plasma, obtained from patients at different stages of cardiopulmonary bypass. RESULTS: Before heparinization, blood diluted with its own platelet poor plasma recorded an impedance change of 13.0 (4.7 to 15.6) Ohms. Platelet poor plasma obtained after heparinization or during extracorporeal circulation reduced this response to 3.7 (1.1 to 8.4) and 2.0 (1.1 to 3.3) Ohms, respectively (both p < 0.0001 versus pre-heparin; n = 13). Macroaggregation in blood from volunteers was similarly inhibited by patients' platelet poor plasma (n = 30). The macroaggregatory response in blood sampled after heparinization for cardiopulmonary bypass, decreased gradually from 11.4 (8.2 to 15.9) Ohms immediately after sampling to 1.7 (1.4 to 4.1) Ohms 2 hours later (p < 0.0001; n = 11). CONCLUSIONS: In vivo heparinization induces plasma changes that inhibit platelet macroaggregation. This is an indirect, delayed inhibition that is transferable in vitro to normal platelets.

Heparin, platelet aggregation, neutrophils, and cardiopulmonary bypass.

UNLABELLED: Cardiopulmonary bypass (CPB) is associated with both neutrophil activation and failure of platelets to form large stable aggregates. We aimed to determine the effects of heparin and of neutrophil activation on platelet aggregation in whole blood. Fourteen patients undergoing routine aortocoronary bypass grafting and NSAID-free for over 7 days were studied before and after heparinisation, and at end-CPB. Whole blood, anticoagulated with rHirudin, was stirred for 3 minutes, and macroaggregation in response to collagen (0.6 microg. mL(-1)) or the neutrophil stimulant fMLP (10(-7)M) was determined by whole blood impedance aggregometry. Microaggregation was measured by counting unaggregated single platelets (corrected for haemodilution). The blood of volunteers was studied in vitro. PATIENTS: Before CPB, heparin effectively abolished platelet macroaggregation induced by collagen (20.5 to 1.4 Ohms) or fMLP (3.9 to 0 Ohms (p<0.0001). CPB had no additional effect. Heparinisation also reduced the platelet count from 127 (110-170) to 95 (64-117). The inhibition of macroaggregation could not be reversed by ex vivo heparinase. VOLUNTEERS: In vitro, the same heparin concentration, as measured in vivo (4 micromL(-1)), inhibited collagen-induced macroaggregation (20.3 to 14.7 Omega), but this effect was less than that observed ex vivo and was reversed by heparinase. In vitro heparin promoted fMLP macroaggregation (2.9 to 8.6 Omega). The inhibition of macroaggregation resulted from heparinisation, per se, rather than CPB and was insensitive to heparinase. There was less inhibition by in vitro heparin, which was reversible by heparinase, indicating a direct effect of heparin in vitro. The disparate findings are suggestive of an indirect action by heparin in vivo on macroaggregation, although heparin had a small direct stimulatory action on microaggregation.

Infective dyspepsia in a heart transplant recipient.

We report the coexistence of symptomatic viral, bacterial, and fungal infection of the upper gastrointestinal tract in a heart transplant recipient. Endoscopic findings were normal at all levels but, because of severe symptoms and recent conversion to positive serology for Cytomegalovirus, biopsies were taken. These showed esophageal candidiasis and gastric Helicobacter infection that has hitherto been unreported in cardiac transplant recipients.

Are we negating the benefits of CABG by forgetting secondary prevention?

UNLABELLED: The objective of the study was to examine medically managed secondary prevention at one year after coronary artery bypass grafting (CABG). In all, 214 consecutive patients undergoing isolated elective CABG seen four weeks preoperatively and one year post-operatively. Preoperative systolic blood pressure averaged 135+/-20 mmHg, which increased to 148+/-25 mmHg (P<0.0001) as did diastolic pressure (81+/-12 to 87+/-13 mmHg; P<0.0001). Anginal symptoms were reported by 45.1% (P<0.0001) although median severity scored lower (4.0 [3.0-5.4] vs 0 [0-2.0]; P<0.0001). Breathlessness decreased from 93% to 64% (P<0.0001) and was scored less severely (4.0 [2.0-5.0] vs 2.0 [0-4.0]; P<0.0001. In all, 88% with postoperative angina reported dyspnoea against 44% of those without (P<0.0001). Calcium antagonist use was more common in patients with angina (27.2% vs 5.1%; P<0.0001), but not nitrates (P=0.8695), diuretics (P=0.4218), digoxin (P=0.2565), beta-blockers (P=0.0820), or ACE inhibitors (P=0.7256). Preoperatively 166 patients (80.2%) took aspirin vs 69.2% afterwards (P=0.0131). Twelve patients (6.5%) received warfarin after operation vs none preoperatively. Two took digoxin (0.97%) preoperatively and 14 (7.7%) postoperatively (P=0.001) for chronic atrial fibrillation. One of these took warfarin. Long-acting nitrate use fell from 63.4% to 15.8% (P <0.0001). Short-acting nitrate use fell similarly (P<0.0001). Preoperatively 37 patients (17.9%) took ACE inhibitors vs 44 postoperatively (24.2%); 39 had not received them before. Preoperatively 48 (23.2%) took diuretics vs 30 (16.5%) postoperatively (P=0.127); 24 had not previously taken diuretics. More patients took HMGCoA inhibitors postoperatively (P=0.0068) and total cholesterol was significantly reduced with a concomitant increase in HDL fraction. Smoking habit was virtually unchanged from 17.8% to 15.1% (P=0.5023). IN CONCLUSION: angina was common. Apart from statin prescribing, postoperative secondary prevention measures were poorly applied, less widespread and less effective than preoperatively. The implications are disturbing.

Antagonism of the platelet 5HT2 receptor in the presence of thrombolysis.

Thrombolysis of coronary arterial thrombi is often accompanied by occlusion due to continued platelet thrombosis. We modified the Folts' model of intracoronary thrombosis (critical stenosis with endothelial damage) to produce up to 35-min occlusions of the circumflex coronary artery in seven open-chest anaesthetised dogs. Administration of recombinant plasminogen activator (rtPA 200 micrograms.kg-1 bolus plus 1 mg.kg-1.h-1 infusion), without heparin or aspirin, always produced effective thrombolysis. Fibrinogen decreased (P < 0.05), thrombin time increased (P < 0.025), bleeding time trebled (P < 0.025) and initial arterial patency was achieved. Addition of a selective 5HT2 antagonist, increased coronary blood flow (P < 0.01) and reduced rethrombosis rate (P < 0.025), but did not affect coagulation or bleeding. The time the vessel spent occluded was significantly decreased (P < 0.01) and correlated with the fibrinogen level (r = 0.97, P < 0.01), thereby implying the presence of fibrin within the thrombus. After rt-PA was withdrawn, bleeding time and fibrinogen level normalised within 30 and 60 min, respectively, but full coronary patency was maintained. Thus, when rt-PA alone had produced full thrombolysis, 5HT2 antagonism prevented intracoronary thrombosis without additional bleeding complications.

Experience of cardiac rehabilitation after coronary artery surgery: effects on health and risk factors.

OBJECTIVE: Cardiac rehabilitation (CR) programs are provided to support the recovery process following acute myocardial infarction and coronary artery bypass grafting (CABG). Attendance varies. We related attendance following CABG to severity of cardiac symptoms, general health status (Short Form-36) and prevalence of modifiable coronary artery disease (CAD) risk factors. METHODS: 209 patients due to undergo CABG were recruited and assessed preoperatively as well as at a mean of 16.4 months postoperatively. General health status was measured using the Short Form-36 questionnaire. Severity of cardiac symptoms was assessed on a visual analogue scale. Modifiable coronary artery disease risk factors (smoking, body mass index, hypertension and elevated cholesterol) and social deprivation index were noted. RESULTS: There were ten early and three late deaths. Thirteen patients withdrew consent for investigation, therefore 183 were fully studied. Of these 65.0% completed a CR programme and 24.6% did not attend any programme; 10.4% partially completed (less than 50% of time) and were excluded from analysis. Nonattenders were more likely to be smokers (P=0.002), diabetic (P=0.028) and were more from socially deprived geographical areas (P=0.013), but the proportion of patients with BMI>25, BP>140/90 or cholesterol >5.0 mmol l(-1) were the same. There were no differences in age, preoperative NYHA score, number of grafts, angina recurrence (46 vs. 38%, P=0.35) or breathlessness (62 vs. 69%, P=0.40) between attenders and nonattenders. The severity scores of angina (2.7 vs. 3.2, P=0.286) and breathlessness (3.5 vs. 3.6; P=0.79) were no different. However, four of the eight health domains measured showed significantly better values for attenders than nonattenders; namely: general health (60 vs. 46%, P=0.001), physical function (64 vs. 51% P=0.01), role limitation physical (48 vs. 29%; P=0.02) and social function 74 vs. 62%, P=0.04). CONCLUSIONS: This is the first report using SF 36 to evaluate benefits from attending CR. Higher general health scores (SF-36) were associated with attendance at CR although CAD risk factors and cardiac symptoms were not improved but this may be due to the long interval between assessments.

Digoxin use in patients awaiting heart transplantation for systolic left ventricular failure.

We reviewed the drug therapy of 83 patients who underwent cardiac transplantation for chronic left ventricular cardiac failure in Scotland from 1992-1996. Digoxin had been prescribed to 52% of patients in sinus rhythm, and 82% of those in atrial fibrillation (P=NS). This audit confirms that, in line with the clinical practice in the period between 1992 and 1996, digoxin was not widely used in patients with advanced chronic heart failure who were in sinus rhythm. The publication of the withdrawal trials in 1993 might have been expected to increase the use of digoxin but this could not be demonstrated. The management of patients on the cardiac transplantation waiting list should include the best symptomatic treatment possible. In view of the clinical and experimental evidence of symptomatic improvement by cardiac glycosides, it is to be hoped that publication of the results of the Digitalis Investigation Group trial will improve this situation.

Platelet aggregation and high-intensity transient signals (HITS) in a sheep model of mitral valve replacement.

BACKGROUND AND AIMS OF THE STUDY: The composition of microemboli detected as high-intensity transient signals (HITS) by Doppler ultrasound in patients with prosthetic heart valves is still debated. Here, platelet aggregation and HITS were investigated in a sheep model. METHODS: Insonation of the carotid artery was performed in 20 sheep with either a mechanical or a biological mitral valve prosthesis in place. The effect of ICI 170809, a 5HT2a antagonist, on the frequency of HITS and on platelet aggregates, counted in arterial blood smears per nine high-power fields, was assessed at three and six months after valve implantation. The mitral transvalvular gradient was measured by transthoracic echocardiography at three and six months. RESULTS: Data are expressed as median and interquartile range. At three months, there were 36 (20-114) HITS/h in the mechanical group, and 0 (0-15) HITS/h in the biological group. At six months, there were 21 (0-82) and 0 (0-2) HITS/h, respectively. The occurrence of HITS was unaffected by either ICI 170809, or by duration of implant in either group. Platelet aggregate counts were higher with the mechanical than with the biological valve at three months, but not at six months. ICI 170809 reduced platelet aggregate counts in both valve types; the reduction was not significant in the bioprosthetic valve group. The pressure gradient across the bioprosthesis increased during the study from 2 (2-3) mmHg to 7.5 (6-10) mmHg, but was unchanged in the mechanical valve. CONCLUSIONS: (i) It was confirmed that the frequency of HITS is higher with the mechanical prosthesis than the bioprosthesis; (ii) circulating platelet aggregates in the bioprosthetic valve group tended to increase as structural valve deterioration occurred; (iii) the frequency of HITS was not influenced by either an increase or a decrease in circulating platelet aggregates; and (iv) HITS detected in patients with prosthetic valves are unlikely to be due to circulating platelet aggregates.

An improved valve rotator.

A device to rotate valve prostheses is described. By using a polythene tubing universal joint the valve may be turned by twisting the handle of the valve rotator without altering its spatial orientation. This modification was designed to facilitate what can be a frustrating manoeuvre and should be applicable to any rotatable valve.