Coronary artery disease in the military patient.

Ischaemic heart disease is the most common cause of sudden death in the UK, and the most common cardiac cause of medical discharge from the Armed Forces. This paper reviews current evidence pertaining to the diagnosis and management of coronary artery disease from a military perspective, encompassing stable angina and acute coronary syndromes. Emphasis is placed on the limitations inherent in the management of acute coronary syndromes in the deployed environment. Occupational issues affecting patients with coronary artery disease are reviewed. Consideration is also given to the potential for coronary artery disease screening in the military, and the management of modifiable cardiovascular disease risk factors, to help decrease the prevalence of coronary artery disease in the military population.

Trends in hospital treatments, including revascularisation, following acute myocardial infarction, 2003-2010: a multilevel and relative survival analysis for the National Institute for Cardiovascular Outcomes Research (NICOR).

OBJECTIVE: To investigate temporal changes in survival after acute myocardial infarction (AMI) by early invasive strategy. METHODS: Accelerated failure time and 6-month relative survival analyses stratified by thrombolysis or primary percutaneous coronary intervention (PPCI) for ST elevation myocardial infarction (STEMI) and coronary angiography for non-STEMI (NSTEMI) encompassing 583 466 patients across 247 hospitals in England and Wales over hospital admission periods 2003-2004, 2005-2006, 2007-2008 and 2009-2010. RESULTS: Survival improved significantly for STEMI patients who received reperfusion therapy (time ratio (TR) 1.47, 95% CI 1.22 to 2.78) and was stable for those who did not (TR 1.02, 95% CI 0.85 to 1.22). While there were significant improvements in survival for NSTEMI patients who underwent coronary angiography (TR 1.39, 95% CI 1.18 to 1.62), there was a significant decline for those who did not (TR 0.70, 95% CI 0.65 to 0.75). Patients without reperfusion therapy or coronary angiography had a greater number of comorbidities, but the use of secondary prevention medications was comparable with patients who received reperfusion therapy or coronary angiography. There was a significant hospital-level survival effect, with higher crude 6-month mortality in hospitals in the lowest coronary angiography and PPCI quartiles (angiography Q1: 16.4% vs Q4: 12.8%; PPCI Q1: 15.8% vs Q4: 12.4%). CONCLUSIONS: Survival rates after AMI have improved. Whereas survival estimates for STEMI patients who did not receive reperfusion therapy were stable, they worsened for NSTEMI patients not receiving coronary angiography.

Percutaneous coronary intervention: recommendations for good practice and training.

Cardiologists undertaking percutaneous coronary intervention (PCI) are excited by the combination of patient and physician satisfaction and technological advance occurring on the background of the necessary manual dexterity. Progress and applicability of percutaneous techniques since their inception in 1977 have been remarkable; a sound evidence base coupled with the enthusiasm and ingenuity of the medical device industry has resulted in a sea change in the treatment of coronary heart disease (CHD), which continues to evolve at breakneck speed. This is the third set of guidelines produced by the British Cardiovascular Intervention Society and the British Cardiac Society. Following the last set of guidelines published in 2000, we have seen PCI activity in the UK increase from 33,652 to 62,780 (87% in four years) such that the PCI to coronary artery bypass grafting ratio has increased to 2.5:1. The impact of drug eluting stents has been profound, and the Department of Health is investigating the feasibility of primary PCI for acute myocardial infarction. Nevertheless, the changes in the structure of National Health Service funding are likely to focus our attention on cost effective treatments and will require physician engagement and sensitive handling if we are to continue the rapid and appropriate growth in our chosen field. It is important with this burgeoning development now occurring on a broad front (in both regional centres and district general hospitals) that we maintain our vigilance on audit and outcome measures so that standards are maintained for both operators and institutions alike. This set of guidelines includes new sections on training, informed consent, and a core evidence base, which we hope you will find useful and informative.

Clopidogrel for prevention of major cardiac events after coronary stent implantation: 30-day and 6-month results in patients with smaller stents.

OBJECTIVES: We developed this study to assess the procedural outcome, complications, and clinical follow-up in patients treated with different antiplatelet regimens after intracoronary stent implantation with small stents. Three hundred sixty-one consecutive patients, in whom at least one 3.0-mm intracoronary stent was implanted, were studied. METHODS: The study was a prospective, observational registry of unselected consecutive patients treated in our institution. Patients who underwent stent implantation between December 1997 and July 1998 were treated with aspirin and ticlopidine; those who received stents between August 1998 and February 1999 were treated with aspirin and clopidogrel. RESULTS: In the group treated with ticlopidine, there were 190 patients who had 253 lesions treated with 274 stents. Mean age was 59.1 years, 72% were male, 31% had unstable angina, 64% had 1 stent, 36% had >1 stent, and 23% had multivessel intervention. In the group treated with clopidogrel, there were 171 patients who had 226 lesions treated with 245 stents. Mean age was 60.4 years, 79% were male, 26% had unstable angina, 70% had 1 stent, 30% had >1 stent, and 26% had multivessel intervention. Complications at 30 days in the ticlopidine group were death in 1 (0.5%), stent occlusion in 3 (1. 6%; all reopened with repeat angioplasty), non-Q-wave myocardial infarction in 2 (1%), and urgent revascularization in 4 (2%). Complications at 30 days in the clopidogrel group were noncardiac death in 1 (1.2%), cardiac death in 1 (1.2%), stent occlusion in 0, non-Q-wave myocardial infarction in 3 (1.8%), and urgent revascularization in 0. Follow-up was available in 100% of patients in both groups (mean 253 +/- 75 days in the ticlopidine group, 198 +/- 53 days in the clopidogrel group). Complications at >30 days in the ticlopidine group were death in 1 and clinical restenosis in 11 (5.8%); 1 additional patient had an admission with unstable angina to the local hospital. Hence, recurrent angina as a consequence of target lesion restenosis occurred in 5.8%. Complications at >30 days in the clopidogrel group were death in 0 and clinical restenosis in 8 (4.7%); 2 additional patients were admitted with unstable angina to the local hospital, and 1 patient had a myocardial infarction 164 days after stent implantation. Hence, recurrent angina as a consequence of target lesion restenosis occurred in 4.7%. There were no significant differences in complications between the 2 groups. CONCLUSIONS: Our observations suggest that clopidogrel can be used instead of ticlopidine in patients treated with stents with a diameter of

Intracoronary Multi-link stents: experience in 218 patients using aspirin alone.

OBJECTIVES: To assess procedural outcome, complications, and clinical follow up in 218 patients who underwent treatment with 297 Multi-link (Guidant) stents implanted without the use of intravascular ultrasound (IVUS) or quantitative coronary angiography (QCA), and using aspirin alone as antiplatelet therapy. METHODS: The case records and angiograms were reviewed and the patients were contacted by telephone to determine their symptoms and any adverse events at follow up. Data were analysed using Fisher's exact test. RESULTS: Of the 218 patients included in the study, 45 had multivessel intracoronary intervention, and 55 had unstable angina. The mean (SD) length of hospital stay following the procedure was 2.0 (2.1) days. There were two early deaths at less than 30 days, and two deaths during follow up at more than 100 days. Ten patients suffered complications during the first 30 days: four had subacute stent thrombosis, of whom two died and two were treated successfully with coronary artery bypass grafting; five had a non-Q wave myocardial infarction; and one had a femoral false aneurysm. Patient outcome was analysed according to stent diameter (3.0 mm or less, or 3.5 mm or more) and by angina status (stable or unstable). In patients in whom at least one stent was 3.0 mm diameter, four of 86 patients suffered acute stent occlusion, whereas in the 132 patients in whom all stents were at least 3.5 mm diameter there were no cases of stent occlusion (p = 0.02). In the unstable angina group two of 55 patients suffered acute stent occlusion compared to two of 163 patients in the stable angina group (NS). In patients with unstable angina and at least one stent of 3.0 mm diameter, the acute occlusion rate was 7.1% (two of 28 patients). Three of the four patients with stent occlusion had undergone complex procedures. Twenty eight patients were restudied for recurrent symptoms during the follow up period. Of these, eight patients had restenosis within their stent. In seven of these patients the stent size was 3.0 mm diameter, and in the remaining patient the stent size was 4.0 mm diameter. Three of the 28 patients restudied had developed new disease remote from the stented site, and 17 had patent stents and no significant other coronary lesion. CONCLUSIONS: This study suggests that coronary intervention using the Multi-link stent is safe and effective using aspirin alone, without IVUS or QCA, when stent diameter is greater than 3.0 mm. All cases of stent occlusion in this series occurred in patients in whom at least one stent was 3.0 mm diameter, with stent occlusion being higher in patients with unstable angina compared to those with stable angina. Additional antiplatelet therapy may be beneficial in those patients in whom Multi-link stent diameter is less than 3.5 mm, particularly in those with unstable angina, but is not necessary for patients receiving Multi-link stents of 3.5 mm diameter or greater.

Planning for coronary angioplasty: guidelines for training and continuing competence. British Cardiac Society (BCS) and British Cardiovascular Intervention Society (BCIS) working group on interventional cardiology.

The following recommendations are made: 1 Existing centres undertaking angioplasty should increase their activity, and the target figure of 400 PTCA procedures per million of the United Kingdom population should be achieved by the end of 1996-97, or immediately thereafter. 2 Angioplasty centres should be appropriately equipped to undertake PTCA safely and effectively and provide a reliable emergency service. They should have a minimum of two trained PTCA operators jointly undertaking a minimum of 200 procedures per year at that centre, and have regular meetings to share experience. 3 Angioplasty operators should ensure that where the need arises patients undergoing PTCA can receive immediate attention from a trained operator at any time until discharge from hospital. 4 Trained operators should undertake at least 1-2 PTCA procedures per week (> 60 procedures per year) to maintain competence, and those undertaking so few procedures should increase their activity over the next three years to more than 100 a year. 5 Trainers should have performed at least 500 procedures before formally training others and should undertake a minimum of 125 procedures a year to maintain accreditation as a trainer. 6 Surgical cover for PTCA procedures should be mandatory and on site cover remains the strongly preferred option. Where surgical cover is provided off site, this should be at a centre less than 30 minutes away by road. Whether provided on or off-site it should be possible to establish cardiopulmonary bypass within 90 minutes of the decision being made to refer the patient for surgery. 7 All operators and interventional centres should audit their activity and results, review these data locally with colleagues, and provide regular audit returns to the national database run by BCIS. This will allow future recommendations concerning standards to take more account of risk stratification and actual outcomes, and not place such emphasis merely on volumes of activity. 8 These recommendations should be reviewed in three years.

Late functional results after surgical closure of acquired ventricular septal defect.

To assess the longer term outlook for patients who have undergone surgery for acquired (postinfarction) ventricular septal defect, we interviewed and studied 60 survivors from a single regional cardiac center between 3 and 144 months after the operation. Including the patients who died within 1 month of the operation, the 5-, 10-, and 14-year survivals (with standard errors) were 69% (65% to 74%), 50% (44% to 57%), and 37% (27% to 46%). Eighty-two percent of patients were in New York Heart Association class I or II. Ten patients (17%) had a persisting but not hemodynamically significant ventricular septal defect. Mean left ventricular ejection fraction was reduced at 0.39 (standard deviation 0.15), but this did not correlate with either New York Heart Association class or exercise tolerance. Twenty-eight patients (47%) had asymptomatic arrhythmias (17 with ventricular premature beats). Angina and other medical problems were not prevalent.

Magnetic resonance angiography in subclavian steal syndrome.

A case is reported of a patient with the subclavian steal syndrome in whom the reversed blood flow of the vertebral artery was shown by phase encoded magnetic resonance angiography.

Left ventricular energetics: heat production by the human heart.

OBJECTIVE: The aim was to examine the effect of coronary artery disease on human left ventricular energetics by a comparison of left ventricular oxygen consumption and heat production. The usefulness of measurement of left ventricular heat production for the detection of the expected change in left ventricular energetics produced by atrial pacing to a faster heart rate was also assessed. METHODS: Forty six patients (mean age 57 years; 31 men) undergoing cardiac catheterisation and coronary arteriography for the investigation of chest pain were studied. Normal left ventricular function and normal coronary arteries were present in eight and 38 had atheromatous coronary artery disease. Left ventricular heat production was calculated from coronary blood flow, the coronary arteriovenous (aorta-coronary sinus) temperature difference, and the areas under thermodilution curves recorded in the aorta and coronary sinus after injection of cold saline into the pulmonary artery. Mean external left ventricular power was calculated from mean arterial blood pressure and cardiac output. Left ventricular mechanical efficiency was derived from heat production and the energy value of myocardial oxygen use, assuming aerobic metabolism. In 27 patients studies were repeated during atrial pacing from the coronary sinus. RESULTS: At rest under basal conditions left ventricular heat production was 2.4(SD 1.0) W in patients with normal hearts and 3.1(1.4) W in patients with coronary disease (NS). Mechanical efficiency was 44.2(9.7)% in the normal patients and 30.7(10.9)% in those with coronary disease (p = 0.003). During atrial pacing to a faster heart rate left ventricular energy supply increased from 4.6(2.7) W to 5.9(3.3) W (p < 0.0005), and heat production increased from 3.0(1.6) W to 4.6(2.4) W (p < 0.0005), but mean external power was not altered. As the extra energy used during pacing was "wasted" as heat, there was a significant fall in left ventricular mechanical efficiency with pacing from 33.9(13.5)% to 18.9(15.2)% (p < 0.0005). CONCLUSIONS: These results show the effect of coronary artery disease on the energetics of left ventricular function. They also show that the method and equipment can detect the expected alteration in left ventricular energetics produced by atrial pacing. The measurement of left ventricular heat production and oxygen consumption allows assessment of the total left ventricular energy flux, and may be useful for the evaluation of drug treatment with such as inotropes and vasodilators, and for the investigation of the functional consequences of left ventricular disease.

Adenosine infusion for the reversal of pulmonary vasoconstriction in biventricular failure. A good test but a poor therapy.

BACKGROUND: Elevation of pulmonary vascular resistance is an important determinant of right ventricular function in patients with end-stage biventricular heart failure. Vasodilator drug therapy directed at the pulmonary vasculature is used in the hemodynamic assessment of patients for orthotopic heart transplantation, and therapy aimed at decreasing pulmonary vascular resistance and transpulmonary pressure gradient has been advocated in patients awaiting heart transplantation. Adenosine infusion has been shown to cause selective pulmonary vasodilatation in normal subjects and in patients with primary pulmonary hypertension but has not been assessed in patients with biventricular heart failure. METHODS AND RESULTS: Using two infusion doses, we studied the pulmonary and renal hemodynamic effects of adenosine on patients referred for heart transplantation (n = 21) and compared it with sodium nitroprusside (n = 18). Patients received 30% oxygen via face mask throughout the study. Adenosine at 100 micrograms/kg min achieved the same percentage fall in pulmonary vascular resistance as nitroprusside (41 +/- 6% versus 42 +/- 4%) and a greater and more consistent fall in transpulmonary pressure gradient (35 +/- 6% versus 9 +/- 30%, p less than 0.02). The mean arterial blood pressure fell by 16 mm Hg with nitroprusside but was unchanged by adenosine, indicating that in contrast to nitroprusside, adenosine acted as a selective pulmonary vasodilator. Despite this, cardiac index showed only a modest increase with adenosine (1.73 +/- 0.09 to 1.89 +/- 0.16 l.m-2, p less than 0.05), and there was a rise in pulmonary capillary wedge pressure from baseline at the higher dose (29.7 +/- 2.5 to 33.4 +/- 3.4 mm Hg, p less than 0.05). Renal blood flow was unchanged during adenosine infusion. CONCLUSIONS: Adenosine is a potent selective pulmonary vasodilator in patients with biventricular heart failure and is preferable to sodium nitroprusside as a test for the reversibility of pulmonary vasoconstriction. However, its deleterious effects on left atrial pressure make it unsuitable as a therapeutic agent in patients awaiting heart transplantation.

Late rupture of a superior intercostal artery following repair of aortic coarctation.

Having had surgical repair of aortic coarctation at the age of 12 years, and re-operation at the age of 19 years for stenosis at the site of the previous repair, a 29 years old man presented as an emergency with a 24 hour history of interscapular pain, haemoptysis and collapse. At thoracotomy he was found to have a ruptured superior intercostal artery which was ligated. Spontaneous rupture of an intercostal artery has not been previously recorded.

Use of computed tomographic scanning and aortography in the diagnosis of acute dissection of the thoracic aorta.

Before the introduction of computed tomographic (CT) scanning, aortography was the investigation of choice for acute aortic dissection. Between 1978 and 1982, 24 patients were referred to the Brompton Hospital with suspected acute thoracic aortic dissection; all had aortography with diagnosis confirmed at surgery (n = 12) or necropsy (n = 2) or supported by clinical outcome (n = 8). One patient in whom aortography was negative had type B dissection at necropsy and another patient was lost to follow up. CT scanning became available in this unit in 1983 and between 1983 and 1987 was used as the only imaging investigation in 32 patients with suspected acute dissection of the thoracic aorta while in a further 22 patients aortography was used alone. Results were confirmed at surgery (n = 18), necropsy (n = 3), or supported by clinical outcome (n = 31). Two patients were lost to follow up. In an additional 16 patients both aortography and CT scanning were performed with concordant findings in 10. In six in whom the results were discordant, aortography was normal in three in whom subsequent CT scanning showed type B dissection and CT scanning was normal in three patients in whom aortography showed type A dissection. Both CT scanning and aortography are reliable techniques for assessment of suspected acute dissection of the thoracic aorta. Both techniques misdiagnose occasionally and the frequency of misdiagnosis will be minimised by performing both investigations in patients where the level of clinical suspicion is high and the initial investigation negative. CT scanning tends to miss type A dissection and in view of the success of surgery in this condition this failing has the more serious clinical consequences.

Clinical correlates of angiographically diagnosed idiopathic pulmonary hypertension.

During 1970-87 43 patients with unexplained pulmonary hypertension (mean pulmonary arterial pressure greater than 25 mm Hg) were admitted to the Brompton Hospital and classified by angiographic criteria as having either symmetrical peripheral pulmonary artery pruning (thought to represent primary plexogenic pulmonary arteriopathy), n = 21, or asymmetrical pulmonary arterial occlusions (thought to represent chronic thromboembolic disease), n = 22. Patients with symmetrical pulmonary arteriopathy had significantly higher mean pulmonary arterial pressures (67 mm Hg) at the time of presentation than those with asymmetrical pulmonary arteriopathy (49 mm Hg). Clinical distinction between these two groups was impossible. Survival from the time of diagnosis was similarly poor in the two groups (26 weeks and 38 weeks) and did not correlate with any of the haemodynamic measurements. The difficulties in making distinctions between these conditions are discussed.

Heat production by the human left ventricle: measurement by a thermodilution technique.

STUDY OBJECTIVE - The aim was to study the feasibility of measuring heat production by the human left ventricle with a view to using this variable as an index of left ventricular mechanical efficiency. DESIGN - The transcoronary temperature difference was derived from catheter mounted thermistors placed percutaneously in the aortic root and coronary sinus. Left ventricular blood flow was measured by continuous thermodilution in the coronary sinus, and heat removal by coronary venous blood was calculated from blood flow and the transcoronary temperature difference. Diffusional heat loss was measured using temperature/time curves recorded in aorta and coronary sinus after a bolus injection of cold saline into pulmonary artery. The heat loss from the system into the endothermic reactions of haemoglobin was calculated from left ventricular oxygen extraction using an assumed respiratory quotient. The energy released by left ventricular myocardial metabolism (EEO2, calculated from oxygen extraction), was compared to measured left ventricular heat production, and the mechanical efficiency of the left ventricle was calculated by the formula: Efficiency = (EEO2 - HLV)/EEO2. PATIENTS - Fifteen conscious patients with anginal chest pain were studied at the time of cardiac catherisation and coronary arteriography. MAIN RESULTS - The transcoronary temperature difference was in the range 0.10-0.32 (mean 0.21) degrees C. Total left ventricular heat production, equal to the sum of heat removed by the blood stream, diffusional loss and endothermic reactions (HLV) was in the range 1.5-4.6 (mean 2.7) watts. The values of EEO2 obtained were in the range 2.4-6.5 (mean 4.0) watts, and the calculated mechanical efficiency of the left ventricle was 0.24-0.55 (mean 0.34). CONCLUSIONS - The measurement of heat production by the human left ventricle is safe and practical. This technique promises to be of value in the clinical investigation of the relationship between myocardial function and energy utilisation.

The clinical features, management and outcome of persistence of the arterial duct presenting in adult life.

We have reviewed the 25 patients who, between 1973 and 1988, presented to the Brompton Hospital in adulthood with persistence of the arterial duct (ductus arteriosus). As pulmonary arteriolar resistance is the main determinant of management and prognosis in this condition, the patients were divided into groups with either normal or mild elevation of resistance (less than 10 units/m2: 19 patients) or with severe elevation (greater than 10 units/m2: 6 patients). Patients with normal pressures or mild elevation tended to be older (mean age 45 years). Many (70%) were asymptomatic, but dyspnoea with signs of left heart failure was the commonest presenting complaint. Surgical closure of the duct was performed in 16 with good result in all. Survival for the entire group, however, was long. There was a symptomatic indication for surgery (due to hyperdynamic circulation) in 5. In those with severely elevated pulmonary arteriolar resistance, the mean age of presentation was 31 years and the survival short. The commonest presenting symptom was dyspnoea. Surgical closure of the duct was attempted in two patients but with a poor outcome in both. All patients with an elevated resistance had developed this complication by the third decade of life. Significant elevation was not a feature of older patients, suggesting that, in this age group, the risk of elevation is slight. Surgery, nonetheless, may be indicated for relief of symptoms due to a large systemic to pulmonary shunt.