Circumstances and mode of in-hospital death in 5750 consecutive patients undergoing percutaneous transluminal coronary angioplasty.
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Biomedical subjects
Publications and source records attributed to R A Perry.
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OBJECTIVE: To assess the cost effectiveness of drug eluting stents (DES) compared with conventional stents for treatment of symptomatic coronary artery disease in the UK. DESIGN: Cost-utility analysis of audit based patient subgroups by means of a simple economic model. SETTING: Tertiary care. PARTICIPANTS: 12 month audit data for 2884 patients receiving percutaneous coronary intervention with stenting at the Cardiothoracic Centre Liverpool between January 2000 and December 2002. MAIN OUTCOME MEASURES: Risk of repeat revascularisation within 12 months of index procedure and reduction in risk from use of DES. Economic modelling was used to estimate the cost-utility ratio and threshold price premium. RESULTS: Four factors were identified for patients undergoing elective surgery (n = 1951) and two for non-elective surgery (n = 933) to predict risk of repeat revascularisation within 12 months. Most patients fell within the subgroup with lowest risk (57% of the elective surgery group with 5.6% risk and 91% of the non-elective surgery group with 9.9% risk). Modelled cost-utility ratios were acceptable for only one group of high risk patients undergoing non-elective surgery (only one patient in audit data). Restricting the number of DES for each patient improved results marginally: 4% of stents could then be drug eluting on economic grounds. The threshold price premium justifying 90% substitution of conventional stents was estimated to be 112 pound sterling (212 USD, 162 pound sterling) (sirolimus stents) or 89 pound sterling (167 USD, 130 pound sterling) (paclitaxel stents). CONCLUSIONS: At current UK prices, DES are not cost effective compared with conventional stents except for a small minority of patients. Although the technology is clearly effective, general substitution is not justified unless the price premium falls substantially.
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We evaluated the current short- and medium-term outcomes of complete revascularization, compared to culprit lesion percutaneous coronary intervention (PCI), in patients with multivessel coronary disease presenting with unstable angina. One hundred fifty-one patients with multivessel coronary disease presented to a tertiary cardiothoracic center with unstable angina/non-ST elevation myocardial infarction (UA/NSTEMI) between January 2000 and September 2001. In group A (n=71), the intended strategy was complete revascularization by multivessel PCI. In group B (n=80), culprit lesion PCI was intended despite the presence of other lesions amenable to PCI (B1) or due to confounding anatomical factors (B2). Clinical variables and endpoints were collected from patient notes, a dedicated database and telephone follow-up, and included recurrent stable and unstable angina, need for repeat PCI or elective coronary artery bypass graft, incidence of non-fatal myocardial infarction (MI) and death. Baseline characteristics were similar in each group. Procedural success was achieved in over 95% of cases in both groups with high stent implantation rates (>96%). There was no observed difference in mortality or incidence of MI between the groups. Compared to group A, more patients in group B1 had residual angina [22.8% (13/57) versus 9.9% (7/71); p=0.041] and required further PCI [17.5% (10/57) versus 7.0% (5/71); p=0.045]. There was a non-significant trend toward fewer readmissions for UA and less long-term antianginal medication in group A [38.0% (27/71) versus 52.6% (30/57); p=0.043]. Complete and culprit lesion revascularization by PCI are safe methods of treating patients with multivessel coronary disease presenting with UA/NSTEMI. Reductions in residual angina, repeat PCI and need for antianginal therapies suggest that complete revascularization should be the strategy of choice when possible.
A 35 year old woman with a long history of intravenous drug abuse presented to a local hospital with severe anaemia, fever, raised markers of inflammation, and positive blood cultures for Staphylococcus aureus. She responded to treatment with antibiotics with improvement in her symptoms and markers of inflammation. Four weeks later a "routine" echocardiogram showed a rupture of her left ventricular apex and a large pseudoaneurysm. There had been no deterioration in her symptoms or haemodynamic status to herald this new development. It was successfully repaired surgically and the patient made a good recovery.
OBJECTIVE: To assess physiological cardiac adaptation in adolescent professional soccer players. SUBJECTS AND DESIGN: Over a 32 month period 172 teenage soccer players were screened by echocardiography and ECG at a tertiary referral cardiothoracic centre. They were from six professional soccer teams in the north west of England, competing in the English Football League. One was excluded because of an atrial septal defect. The median age of the 171 players assessed was 16.7 years (5th to 95th centile range: 14-19) and median body surface area 1.68 m(2) (1.39-2.06 m(2)). MAIN OUTCOME MEASURES: Standard echocardiographic measurements were compared with predicted mean, lower, and upper limits in a cohort of normal controls after matching for age and surface area. Univariate regression analysis was used to assess the correlation between echocardiographic variables and the age and surface area of the soccer player cohort. ECG findings were also assessed. RESULTS: All mean echocardiographic variables were greater than predicted for age and surface area matched controls (p < 0.001). All variables except left ventricular septal and posterior wall thickness showed a modest linear correlation with surface area (r = 0.2 to 0.4, p < 0.001); however, left ventricular mass was the only variable that was significantly correlated with age (r = 0.2, p < 0.01). Only six players (3.5%) had structural anomalies, none of which required further evaluation. All had normal left ventricular systolic function. Sinus bradycardia was found in 65 (39%). The Solokow-Lyon voltage criteria for left ventricular hypertrophy were present in 85 (50%) and the Romhilt-Estes points score (five or more) in 29 (17%). Repolarisation changes were present in 19 (11%), mainly in the inferior leads. CONCLUSIONS: Chamber dimensions, left ventricular wall thickness and mass, and aortic root size were all greater than predicted for controls after matching for age and surface area. Sinus bradycardia and the ECG criteria for left ventricular hypertrophy were common but there was poor correlation with echocardiographic left ventricular hypertrophy. The type of hypertrophy found reflected the combined endurance and strength based training undertaken.
Although contrast angiography is important in the diagnosis and treatment of atherosclerotic disease, it does have limitations. Intracoronary ultrasound more accurately assesses the amount of atherosclerosis and has given us new insights into the pathophysiology of coronary plaque accumulation and remodelling. It also allows the monitoring of therapeutic intervention. Intracoronary ultrasound is a new gold standard. It does not obviate the need for angiography but provides complementary information that enables us to perform optimal interventional procedures.
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We describe the setting up of a 'heart emergency centre' linked to a pre-existing coronary care unit. The 'heart emergency centre' offers a new and efficient way of providing a fast and effective system for the assessment and management of patients with cardiac emergencies. This set-up can result in significant improvements in 'door to needle' time for thrombolysis, which has been shown to be beneficial both in terms of morbidity and mortality following myocardial infarction.
BACKGROUND: The exact mechanism that explains the phenomenon of cold intolerance in patients with angina remains controversial. Although the response to the effects of a cold environment has been examined in these patients, their response to cold air inhalation has produced conflicting results. In addition, the possible role of vasoactive peptides in the pathophysiology has not been explored. OBJECTIVES: The aims of this study were to examine the response of patients with stable angina to the effects of cold air inhalation during exercise testing, and to investigate the possible role played by the vasoconstrictor peptides endothelin-1 (ET-1) and angiotensin-II (AT-II) in the pathophysiology. METHODS: In a randomised order, 12 men with stable angina, whose medication had been stopped, underwent two separate symptom limited treadmill exercise tests. At one visit the patients exercised while breathing room air and at the other visit they exercised while breathing cold air from a specially adapted freezer. Serial peripheral venous blood samples were taken for ET-1 and AT-II estimations during each visit. RESULTS: Cold air inhalation resulted in a significant reduction in the mean time to angina (232.7 (20.4) s v 274.1 (26.9) s, P = 0.04) and the mean total exercise time (299.5 (27.0) s v 350.3 (23.9) s, P = 0.008), but no significant change in the time to 1 mm ST depression (223.3 (29.0) s v 241.3 (29.2) s, P = 0.25). There was no significant difference between the rate-pressure products at the onset of angina (P = 0.13) and the time to 1 mm ST depression (P = 0.85), but at peak exercise the rate-pressure product was significantly lower in patients breathing cold air as opposed to room air (P = 0.049). There was an equivalent significant decrease in ET-1 concentrations at peak exercise compared with that at rest at both visits (room air 5.0 (0.7) pmol/l v 4.3 (0.7) pmol/l, P = 0.03; cold air 4.4 (0.6) pmol/l v 3.8 (0.5) pmol/l, P = 0.02). There was a significant increase in AT-II concentrations 10 min after peak exercise in patients breathing room air (39.2 (6.1) pmol/l v 32.1 (4.8) pmol/l, P = 0.01) which was not repeated during cold air inhalation (36.6 (3.4) pmol/l v 28.3 (3.4) pmol/l, P = 0.07). CONCLUSIONS: Cold air inhalation in patients with stable angina results in an earlier onset of angina and a reduction in exercise capacity. Both peripheral and central reflex mechanisms appear to contribute to the phenomenon of cold intolerance. Peripheral ET-1 and AT-II do not appear to play a significant role in the pathophysiology.
OBJECTIVE: To evaluate which Doppler transmitral velocity indices of left ventricular diastolic function change with alteration of left ventricular filling pressure. METHODS: Twenty-two patients undergoing coronary artery bypass surgery. The effect of fluid loading on indices derived from the transmitral Doppler waveform, recorded by a trans-oesophageal echocardiography, was evaluated using a generalised linear statistical model. RESULTS: E-wave maximum velocity, E-wave acceleration time and slope, E-wave deceleration slope, A-wave maximum velocity and E/A wave maximum velocity ratio showed significant changes after alterations in left ventricular filling pressure. E-wave deceleration time and E-wave maximum velocity/time velocity integral showed no significant change after fluid loading. CONCLUSION: Several commonly used Doppler derived indices of left ventricular diastolic function are significantly affected by changes in filling pressure of the left ventricle. This may limit the usefulness of the Doppler method for serial assessment of diastolic function when the left ventricular filling pressure has changed between assessments. Only the E-wave deceleration time did not show significant changes and might be a useful Doppler index for the serial measurement of left ventricular compliance but this needs to be confirmed with haemodynamic measurements.
We describe direct and quantitative evidence of free-radical production in the early stage after recanalisation in a patient undergoing primary coronary angioplasty for acute myocardial infarction. After successful initial dilation, the procedure was complicated by re-occlusion of the artery at the same site, with subsequent fall in free-radical generation. After repeat angioplasty, recanalisation was again accompanied by increased free-radical production.
BACKGROUND: Free-radical generation after successful thrombolysis in acute myocardial infarction may jeopardize ischaemic but viable myocardium, thus limiting the optimal benefits of reperfusion. METHODS: Circulating free-radical activity was assessed in 25 consecutive patients with acute myocardial infarction. Those who successfully reperfused (Group A) were compared with those who did not (Group B). We also compared patients who had or had not developed Q waves and patients with and without previous angina or myocardial infarction. All patients presented within 6 h of the onset of chest pain and received standard intravenous streptokinase therapy. Free-radical activity in serial serum samples collected over 72 h was measured using the percentage molar ratio (PMR) of the concentrations of 9,11-linoleic acid to 9,12-linoleic acid, and malonaldehyde concentration. RESULTS: Throughout the study period Group A (n = 11) showed significantly greater change in serum PMR and malonaldehyde levels compared with Group B (n = 14) (P < 0.01). PMR differences between the two groups were most pronounced at 3 and 12 h (P < 0.001). Patients with non-Q-wave myocardial infarction (n = 5) showed significantly greater changes in serum PMR and malonaldehyde levels (P < 0.01) compared with those with Q-wave infarction (n = 20). A history of previous infarction or angina had no apparent effects on the changes in serum free-radical activity. CONCLUSIONS: Successful early reperfusion and non-Q-wave myocardial infarction are both associated with a significantly greater increase in the levels of markers of serum free-radical activity immediately after infarction. The results support present concepts of free-radical-mediated reperfusion injury. Use of these assays may identify those patients who may be at risk from free-radical-mediated reperfusion injury.
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A 45 year old farmer was kicked in the chest by a horse. In the days following the injury episodic breathlessness developed and he was admitted to hospital with right ventricular failure and pulmonary emboli. Echocardiography showed global right ventricular dysfunction but a right ventricular mural thrombus, the likely source of the pulmonary emboli, was not seen. He gradually recovered after treatment with anticoagulant. One month later he presented with a further complication--complete atrioventricular dissociation--that required a dual chamber pacemaker implantation. This patient had few initial manifestations of right ventricular myocardial contusion and this case illustrates that such patients should be closely monitored for delayed complications.
In order to determine whether cortisol acts directly at the level of the fetal pituitary to promote pars distalis corticotroph maturation, we have infused cortisol into the hypothalamo-pituitary-disconnected (HPD) fetal sheep from 111 to 117 days of gestation. In this study we have measured fetal plasma cortisol and immunoreactive adrenocorticotrophic hormone (ir-ACTH) concentrations between 105 and 116 days of gestation, and we have determined the proportions of adult- and fetal-type corticotrophs in the pars distalis of catheter control fetuses and in HPD fetuses infused with either saline (HPD+SAL) or cortisol (2 mg/day; HPD+F). The fetal plasma cortisol concentrations did not change significantly following HPD. The mean fetal plasma cortisol concentration between 113 and 116 days was threefold higher in the HPD+F fetuses than that measured in HPD fetuses. Following HPD, fetal plasma ir-ACTH concentrations were significantly higher than in catheter control fetuses. Despite the significant elevation in plasma cortisol concentrations in HPD+F fetuses between 113 and 116 days, plasma ir-ACTH concentrations were not different in these fetuses from HPD fetuses infused with saline. At 117 days of gestation in HPD+F fetuses, the proportion of fetal-type corticotrophs in the pars distalis was significantly less than in the HPD+SAL fetuses; however, there was no significant change in the proportion of adult-type corticotrophs in the pars distalis following cortisol infusion. We have shown that cortisol has a direct trophic effect on the maturation of the pars distalis corticotrophs; however, the full maturation of these cells requires an intact hypothalamo-pituitary axis. These findings demonstrate the importance of the fetal hypothalamus in anterior pituitary corticotroph maturation during the last third of gestation.
Electron microscopy was used to assess the cytological maturity of the zona fasciculata cells in the adrenal cortex of fetal sheep at 105 days of gestation, following several ACTH infusion regimes. The aim of this study was to correlate the morphological appearance of the fetal adrenal zona fasciculata cells with the expression of the steroid hydroxylase genes and the fetal plasma cortisol concentrations in a parallel study. Immediately following infusion of ACTH for 24 or 72 h, the zona fasciculata cells at the cortico-medullary junction were more mature than those in the saline-infused controls. When ACTH infusions were withdrawn for 24-72 h prior to the termination of the experiment, the deep cortical cells appeared less mature than those in fetuses which had received ACTH right up until the time of tissue collection. Following ACTH administration, mitochondrial changes preceded changes in the smooth endoplasmic reticulum, and when ACTH was withdrawn, the smooth endoplasmic reticulum responded before the mitochondria. The study demonstrated a correlation between the cytological maturity of the deep zona fasciculata cells and the expression of the genes for the steroidogenic enzymes P-450(17)alpha and P-450scc in the 105-day fetal sheep adrenal following ACTH infusion.
A theoretical formula for calculation of peak dP/dt was derived using parameters obtained from continuous wave Doppler echocardiography signals of aortic blood flow. The direct proportional relationship between the main variables of this formula and invasively measured peak dP/dt was validated in 20 patients undergoing routine diagnostic cardiac catheterization. Doppler signals of aortic flow were obtained simultaneously to invasive pressure recordings with a 2 MHz continuous wave transducer via the suprasternal echocardiographic window. The Doppler signals were recorded on magnetic tape and measurements were made with digital calipers by two independent, blinded observers. The following parameters were measured: peak velocity (V) and time from onset of ejection to peak velocity (T). V2/T, the variable of the derived formula, was calculated for each of the observer's measured parameters and showed a very high interobserver correlation. The two observers' measurements of each parameter were averaged for each patient and the resulting mean was used in calculating the V2/T and mean acceleration. 4. A good correlation of V2/T with invasively measured peak dP/dt was obtained. Our derived index of left ventricular function showed a higher correlation with peak dP/dt compared to other Doppler indices of ventricular function. V2/T may provide a noninvasive method for estimating peak dP/dt.