Primary percutaneous coronary intervention for acute ST elevation myocardial infarction--first year's experience of a tertiary referral centre in the UK.

This study evaluated the first year's experience of a large interventional centre in the UK after a primary percutaneous coronary intervention (PCI) programme that runs 24 hours a day and seven days a week was started. Workload, patient outcome, length of stay, and effect on the remainder of the interventional service were analysed. The primary PCI service for a mainly urban population of 800,000 was started in April 2005. All relevant characteristics, details of procedures, outcome, and other data on quality of care were collected and entered prospectively onto a computerised database. Data were analysed with SPSS (version 13.0). Over a 12-month period, 305 patients were diagnosed with ST elevation myocardial infarction (STEMI), of whom 259 (85%) were accepted for primary PCI. Median door-to-balloon time was 98 minutes, which decreased from 106 minutes in the first six months to 93 minutes in the second six months (p < 0.005). In-hospital mortality was 4.5% and 30-day mortality was 4.9%. Median length of stay was three days, which was reduced from the six days previously reported after thrombolysis. Waiting times for other acute and elective PCI procedures did not increase after initiation of the primary PCI programme. Primary PCI can be delivered successfully in a setting in the UK with low mortality and reduced length of stay and without a negative impact on other interventional services.

Effect of captopril, an angiotensin-converting enzyme inhibitor, in patients with angina pectoris and heart failure.

The effects of captopril and placebo were compared in 18 patients with chronic heart failure and angina pectoris with use of a double-blind crossover trial design. Symptoms were assessed by patient treatment preference, visual analogue scores and nitroglycerin consumption. Exercise performance was assessed using two different treadmill protocols of different work intensity with simultaneous measurement of oxygen consumption and by supine bicycle exercise and simultaneous radionuclide ventriculography. Arrhythmias were assessed by 48 h ambulatory electrocardiographic monitoring. Patients generally preferred placebo to captopril, and this appeared to be due to an increase in symptoms of angina with captopril. Treadmill exercise time on a high intensity protocol was shorter with captopril than with placebo; on a low intensity protocol, angina became a more frequent limiting symptom even though overall exercise performance was not changed. The heart rate-blood pressure product was reduced, but largely because of a reduction in blood pressure rather than in heart rate. During supine bicycle exercise, no differences in symptoms, exercise performance, ejection fraction or changes in blood pressure were noted and ventricular arrhythmias were reduced. Captopril does not appear to be clinically useful in alleviating angina pectoris in patients with heart failure, and this effect may be related to a decrease in coronary perfusion pressure. Nonetheless, desirable metabolic effects, a reduction in arrhythmias and potential effects on survival require further study of captopril in patients with both angina and heart failure.

Left ventricular hypertrophy and mortality in hypertension: an analysis of data from the Glasgow Blood Pressure Clinic.

Three thousand seven hundred and eighty-three patients with non-malignant hypertension attending the Glasgow Blood Pressure Clinic between 1968 and 1983 were followed prospectively for an average of 6.5 years. Left ventricular hypertrophy (LVH) was present at the outset in 34.5% of the men, and 12.8% had ST-T changes. The corresponding figures for women were 21.5% and 8.8%. The prevalence of LVH increased with the severity of hypertension and was higher for a given blood pressure level in men than in women. All-cause age-adjusted mortality, expressed as deaths per 1000 patient-years, was 27.6 for men with normal electrocardiographs, 43.2 for men with LVH only (P less than 0.001) and 56.9 for men with LVH and ST-T changes (P less than 0.001). Similar trends were seen in women. The excess risk associated with LVH, with or without ST-T changes, could not be explained by age, increased blood pressure at referral to the clinic, or smoking habit, when these factors were considered either separately or in combination (regression analysis). Thus, our study demonstrates that LVH, with or without ST-T changes is an independent risk factor for mortality in hypertensive patients.

A review of rhythm disorders in cardiac hypertrophy.

Ventricular arrhythmias frequently occur in both experimental and human left ventricular hypertrophy. The mechanism of arrhythmia is not clear but appears to be related to the process of hypertrophy and the accompanying fibrosis rather than to coexistent coronary artery disease or diuretic-induced hypokalemia. Although neither the independent prognostic value of ventricular arrhythmias nor the benefit of antiarrhythmic therapy has been demonstrated in prospective studies involving hypertensive patients, it is possible that appropriate antiarrhythmic therapy may reduce mortality in selected patients with severe hypertrophy.

Atenolol and celiprolol for stable angina pectoris.

Once-daily atenolol and celiprolol were compared in a placebo-controlled crossover study of 16 patients with stable angina pectoris. Atenolol and celiprolol equally and significantly reduced frequency of angina and electrocardiographic evidence of cardiac ischemia. Celiprolol, however, produced less suppression of the double product at 1 mm of ST-segment depression than atenolol, suggesting that actions other than reduction of heart rate may contribute to its antianginal efficacy.

Left ventricular hypertrophy as a factor in arrhythmias and sudden death.

Hypertensive patients with left ventricular hypertrophy (LVH) are predisposed to sudden cardiac death. Several studies have demonstrated that complex ventricular arrhythmias, including episodes of nonsustained ventricular tachycardia, occur commonly during ambulatory electrocardiographic monitoring of hypertensive patients with LVH. The prognostic significance of such arrhythmias is not known. In other forms of cardiac hypertrophy, however, such as hypertrophic cardiomyopathy, complex ventricular arrhythmias detected during ambulatory monitoring are predictive of subsequent sudden death and there is some evidence that appropriate antiarrhythmic drug therapy may reduce mortality.

Ventricular arrhythmias in hypertensive left ventricular hypertrophy. Relationship to coronary artery disease, left ventricular dysfunction, and myocardial fibrosis.

Ventricular arrhythmias occur with increased frequency in hypertensive patients with left ventricular hypertrophy (LVH). The relationships, however, between ventricular arrhythmias and coexistent coronary artery disease, left ventricular dysfunction and left ventricular fibrosis have not been examined in hypertensive LVH. We carried out coronary arteriography on fifteen hypertensive patients with LVH and nonsustained ventricular tachycardia (greater than or equal to 3 consecutive ventricular complexes) of whom nine (60%) were free of significant (greater than 50% stenosis) coronary disease. To identify other possible correlates of left ventricular arrhythmias, 28 patients with LVH, comprising 17 with ventricular tachycardia and 11 without ventricular arrhythmias, underwent quantitative assessment of left ventricular function (angiographic ejection fraction), left ventricular mass (echocardiography), and left ventricular fibrosis (endomyocardial biopsy). Ejection fraction was not significantly different between the two groups (53 +/- 8% v 62 +/- 2%, P = NS). However, left ventricular mass was significantly greater (442 +/- 28 g v 339 +/- 34 g, P less than .05) and percentage fibrosis significantly higher (19 +/- 4% v 3 +/- 1%, P less than .001) in those patients with ventricular tachycardia. Thus ventricular arrhythmias in hypertensive patients with LVH cannot be entirely attributed to coexistent coronary disease, nor to left ventricular dysfunction, but are related to the degree of cardiac hypertrophy and subendocardial fibrosis.

Haemostatic and haemodynamic abnormalities associated with left atrial thrombosis in non-rheumatic atrial fibrillation.

OBJECTIVE: To evaluate the role of haemostatic and haemodynamic variables in left atrial thrombosis in non-rheumatic atrial fibrillation. DESIGN: Case-control study. SUBJECTS: One hundred and nine patients with non-rheumatic atrial fibrillation. INTERVENTIONS: Peak blood velocity measured at three sites in the left atrium. Venous blood sampled for coagulant proteins and markers of haemostatic activation. MAIN OUTCOME MEASURES: Presence of left atrial thrombus and spontaneous echo contrast at transoesophageal echocardiography. RESULTS: Left atrial thrombus was identified in 19 patients (18%), 16 of whom had spontaneous echo contrast. Patients with thrombus had reduced peak left atrial appendage velocity compared with those without (0.17 v 0.26 m/s; P < 0.001), but no significant reductions in peak mid-left atrial or mitral valve outflow velocity. Patients with thrombus had increased plasma markers of platelet activation-beta thromboglobulin (56.8 v 30.4 IU/ml; P < 0.001) and platelet factor 4 (6.1 v 3.5 IU/ml; P < 0.01)-and of thrombogenesis: thrombin-antithrombin complexes (5.59 v 3.06 micrograms/ml; P < 0.001) and D-dimers (479 v 298 ng/ml; P < 0.01). von Willebrand factor was also increased (1.81 v 1.52 IU/ml; P < 0.05). A multiple logistic regression model identified left atrial appendage velocity (P = 0.001), beta thromboglobulin (P = 0.002), and von Willebrand factor (P = 0.04) as the independent associates of left atrial thrombosis, ahead of the presence of spontaneous echo contrast. CONCLUSIONS: Haemostatic and haemodynamic abnormalities are associated with left atrial thrombus in non-rheumatic atrial fibrillation, and may help stratify thromboembolic risk.

High blood pressure in the Western Isles: a comparative study with Dundee.

A screening programme for cardiovascular risk factors in men aged 50-59 was undertaken in North Uist, and the results compared with an age- and sex-matched control group from Dundee screened as part of the Scottish Heart Health Study. Blood pressure levels were higher in the Islanders than in controls (148 +/- 20/89 +/- 10 mmHg vs 134 +/- 19/84 +/- 11 mmHg (P less than 0.001). Analysis of standard twelve-lead electrocardiograms revealed a greater prevalence of left ventricular hypertrophy in the Islanders (51% vs 16%, P less than 0.005), suggesting that the recorded BP differences were real and not artefacts of measurement. The explanation for the higher BP on North Uist is less clear. Environmental factors that might influence BP including body mass index, the amount of exercise taken, alcohol consumption, dietary salt and potassium intake were similar in North Uist and Dundee. By contrast, an analysis of family names in the two centres indicated a greater degree of common ancestry in North Uist (28 surnames/84 islanders v 98 surnames/110 controls, P less than 0.001). These results suggest that known environmental causes of hypertension are not responsible for higher BP amongst men of North Uist, and this with the data on family names raises the possibility that genetic factors are more important.

Double-blind randomised placebo-controlled dose-efficacy study of sustained release verapamil in chronic stable angina.

The efficacy and tolerability of sustained release verapamil (Securon SR) was investigated in twenty-four patients with chronic stable angina. Patients entered four randomised, double-blind treatment periods, each lasting one week of verapamil-SR 240 mg once daily, 360 mg once daily, 240 mg twice daily, and matching placebo. Four patients were withdrawn, but in one instance this was attributable to side effects from verapamil. Among the remaining twenty patients, mean frequency of angina fell from 4.25 episodes during the last five days of placebo to 2.35, 2.6 and 1.3 episodes during respective active treatments (all P less than 0.001). Compared with placebo the median percentage increase in time to 1 mV ST depression during treadmill exercise (12 hours post dose) was significant only with the regimen of verapamil-SR 240 mg given twice daily at +11% (P = 0.04). Total duration of exercise was also significantly longer and maximum ST depression significantly less only with the twice daily treatment (704 + 186 sec vs 648 + 203 sec; P = 0.03, and 1.75 + 0.73 mm vs 2.15 +/- 0.62 mm; P = 0.02). Side effects, predominantly constipation, breathlessness, and swollen ankles, occurred most frequently with verapamil-SR 360 mg. Thus, sustained release verapamil is well tolerated and effective in the treatment of angina. A regimen of 240 mg given twice daily emerges as superior to once daily treatments for 24-hour prophylaxis of angina.

Haemodynamic performance of a 16-mm Carbomedics aortic prosthesis.

A 55-year-old lady underwent repeat aortic valve replacement using a 16-mm Carbomedics prosthesis. She made an uneventful postoperative recovery and now leads an unrestricted life. Doppler echocardiography reveals a 21-mm Hg gradient across the valve at rest. This did not increase with an infusion of 30 mcg/kg per min of dobutamine, which resulted in an increase in the cardiac output from 1.96 to 5.46 l/min.

Celiprolol and atenolol in angina--effects on left ventricular function.

Celiprolol, 400 mg once daily, and atenolol, 100 mg once daily, were compared in a double-blind placebo-controlled crossover study of 16 patients with stable angina. Both drugs reduced angina frequency and delayed the onset of ischaemia during exercise, although only celiprolol prolonged exercise time. Celiprolol produced less suppression of heart rate than atenolol during exercise, and atenolol, but not celiprolol, lowered resting and exercise cardiac output. Thus, the ancillary properties of celiprolol, including partial beta 2-adrenoceptor agonist activity and direct vasodilating activity, have detectable effects on cardiac function that may be beneficial in patients with angina.

Determinants of ventricular arrhythmias in cardiac hypertrophy.

Ventricular arrhythmias occur with increased frequency in both experimental and human cardiac hypertrophy. Although the process of hypertrophy itself may be arrhythmogenic, other factors may contribute to the high prevalence of arrhythmias in hypertensive patients with left ventricular hypertrophy (LVH). Disease of the large epicardial coronary arteries or of the small intramyocardial vessels (coronary microangiopathy) may lead to myocardial ischemia and thus predispose to arrhythmia. Myocardial fibrosis, a common sequelae of cardiac hypertrophy, has also been shown to be associated with ventricular arrhythmias in experimental models. Other possible determinants of ventricular arrhythmias in this group of patients include metabolic abnormalities; studies relating to the importance of hypokalemia in particular have yielded conflicting results. Thus a number of factors may combine to explain the high prevalence of ventricular arrhythmias in hypertensive patients with LVH.

Importance of ancillary properties of beta blockers in angina: a study of celiprolol and atenolol.

Celiprolol (400 mg) and atenolol (100 mg) were given once a day to 16 patients with stable angina pectoris in a double blind placebo controlled crossover study. Celiprolol produced less suppression of heart rate both at rest and during exercise than atenolol. Both drugs were equally effective in reducing the frequency of angina and in delaying the onset of ischaemia during exercise. Radionuclide ventriculography showed that atenolol but not celiprolol lowered cardiac output at rest and during exercise. Thus the ancillary properties of celiprolol, including partial beta 2 agonist activity and direct vasodilating activity, have detectable effects on cardiac function that may be beneficial in patients with angina.

Gas gangrene in intestinal angina.

A patient with Clostridium welchii infection complicating intestinal angina is reported. Surgical resection of bowel of dubious viability is important to avoid this unusual complication.

Angina, ischemia, and effort tolerance with vasodilating beta-blockers.

beta-Blockers are known to suppress exercise-induced ischemia but give rise to such problems as fatigue or dyspnea on effort and also bradycardia. In a series of double-blind, placebo-controlled studies of celiprolol (a cardioselective beta 1-blocker with beta 2-agonist and vasodilatory properties) in patients with hypertension and angina and in normal volunteers, it was found that celiprolol did not produce bradycardia when given in combination with verapamil. Celiprolol did reduce exercise-induced ischemia, but there was no reduction in cardiac output at rest or on exercise compared with placebo. Compared with atenolol, celiprolol produced less dyspnea and fatigue at submaximal levels of exercise. It is concluded that celiprolol possesses certain differences, compared with conventional beta-blockers, that may be of direct clinical benefit.

Electrocardiographic diagnosis of left ventricular hypertrophy: influence of body build.

1. The sensitivity and specificity of four sets of electrocardiographic criteria for detection of left ventricular hypertrophy were evaluated in an echocardiographic study of 100 hypertensive patients. 2. All criteria gave reasonable specificity (87-94%) but poor sensitivity (39-52%). 3. When non-obese and obese patients were studied separately, criteria based on chest lead voltages were more sensitive than limb lead criteria for detection of left ventricular hypertrophy in non-obese subjects; however, the reverse was true in obese hypertensive patients, where criteria based on limb lead voltages were more sensitive than chest lead voltage criteria. 4. These data suggest that stratification of subjects by body build might improve the diagnostic performance of the electrocardiogram for detection of left ventricular hypertrophy.

Feasibility and applicability of coronary stent implantation with the direct brachial approach: results of a single-center study.

Implantation of stents in selected patients improves outcome after coronary angioplasty. Newer antiplatelet regimes limit access site complications associated with stenting by the percutaneous femoral approach, but a substantial proportion of patients will require anticoagulant therapy for concomitant disease or will have peripheral vascular disease that prevents access from the leg. We investigated procedural success rates and outcome in consecutive patients undergoing elective stent implantation in our institution. In 73 patients who were receiving anticoagulation therapy and were stented by a direct approach to the left brachial artery, 98.6% of stents were successfully deployed, with a major vascular access site complication rate of 1.4%. Equipment consumption, procedural success rate, and fluoroscopy time were similar in patients stented by the direct brachial or percutaneous femoral approach. Where the percutaneous femoral approach is precluded or patients are anticoagulated, stent procedures can be successfully performed by the direct brachial approach with a low rate of access site complications, even when large-caliber guiding catheters are required.