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ACC/AHA 2008 Performance Measures for Adults With ST-Elevation and Non-ST-Elevation Myocardial Infarction

ACC/AHA 2008 Guidelines for the Management of Adults With Congenital Heart Disease
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J Am Coll Cardiol, 1998; 32:2018-2022
© 1998 by the American College of Cardiology Foundation
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CLINICAL STUDIES

Clinical characteristics determining the mode of presentation in patients with acute coronary syndromes

Simon Kennon, MB, MRCP*, Abdul Suliman, MB, MRCP{ddagger}, Peter K. MacCallum, MD, MRCPath{dagger}, Kulasegaram Ranjadayalan, MPhil, MRCP{ddagger}, Paul Wilkinson, MB, MRCP§ and Adam D. Timmis, MD, FRCP*

* Department of Cardiology, Royal Hospitals Trust, London, United Kingdom
{dagger} Department of Haematology, Royal Hospitals Trust, London, United Kingdom
{ddagger} Department of Cardiology, Newham Healthcare Trust, London, United Kingdom
§ Department of Environmental Epidemiology, London School of Hygiene and Tropical Medicine, London, United Kingdom

Manuscript received April 7, 1998; revised manuscript received July 27, 1998, accepted August 6, 1998.

Address for correspondence: Dr. Adam D. Timmis, Royal Hospitals Trust (London Chest Hospital), Bonner Road, London E2 9JX, United Kingdom


   Abstract
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Objectives. The purpose of this study was to examine clinical characteristics of patients with acute coronary syndromes to identify factors that influence the mode of presentation.

Background. In acute coronary syndromes, presentation with myocardial infarction or unstable angina has major prognostic implications, yet clinical factors affecting the mode of presentation are not well defined.

Methods. A prospective cohort study was made of 1,111 patients with acute coronary syndromes. Baseline demographic, clinical and biochemical data were compared in groups with myocardial infarction (n = 633) and unstable angina (n = 478).

Results. The risk of myocardial infarction relative to unstable angina was increased by age >70 years (odds ratio [OR] 2.21; 95% confidence interval [CI] 1.33 to 3.66), male gender (OR 1.56; CI 1.13 to 2.16) and cigarette smoking (OR 1.49; CI 1.09 to 2.03). A rise in admission creatinine from the 10th to the 90th centile of the distribution also increased the odds of myocardial infarction (OR 1.30; CI 1.05 to 1.94). Conversely, the risk of myocardial infarction relative to unstable angina was reduced by previous treatment with aspirin (OR 0.37; CI 0.27 to 0.52), hypertension (OR 0.64; CI 0.47 to 0.86) and previous acute coronary syndromes (OR 0.36; CI 0.26 to 0.51) and revascularization procedures (OR 0.36; CI 0.21 to 0.62).

Conclusions. The clinical presentation of acute coronary syndromes may be influenced by various factors that have the potential to influence the coagulability of the blood, the collateralization of the coronary circulation and myocardial mass. Myocardial infarction is favored by cigarette smoking, advanced age and renal impairment, while unstable angina is favored by treatment with aspirin, hypertension, previous revascularization and previous coronary syndromes.

Abbreviations and Acronyms
  CABG = coronary artery bypass grafting
  PAI-1 = plasminogen activator inhibitor

The importance of plaque rupture and thrombosis in the pathogenesis of acute coronary syndromes is well established, presentation with myocardial infarction or unstable angina depending largely on whether the thrombus is occlusive or subocclusive (1–3). This in turn is related to the degree of plaque disruption and the magnitude of the thrombotic response as determined by the balance between local prothrombotic and antithrombotic activity (4). Major physiologic contributors to this equilibrium are the vascular endothelium and the coagulation cascade, which interact to regulate platelet function, lytic activity, thrombin production and vascular tone (5).

Modification of the thrombotic response to plaque rupture plays a major role in management of acute coronary syndromes. Thrombolytic therapy and aspirin help restore coronary patency in acute myocardial infarction, permitting reperfusion of the ischemic zone (6), while heparin and aspirin protect against thrombotic occlusion in unstable angina (2,3). Treatments of this type, applied after the plaque event, have significantly improved the prognosis of these acute coronary syndromes by reducing or protecting against irreversible myocardial injury (7,8).

If therapeutic modification of thrombotic responses to plaque rupture can favorably influence the natural history of acute coronary syndromes, it is possible to speculate that the mode of presentation might itself be influenced by the balance between prothrombotic and antithrombotic activity that obtains at the time of the plaque event. Thus, Garcia-Dorado et al. have reported that patients with acute coronary syndromes who are taking aspirin are more likely to present with unstable angina than myocardial infarction, suggesting that aspirin taken before the plaque event might attenuate the severity of the thrombotic response (9). In the present study we have prospectively logged the demographic and clinical characteristics of a consecutive series of patients with acute coronary syndromes to identify factors influencing the mode of presentation.


   Methods
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Patient population.   Between January 1995 and December 1997, 1,200 patients were admitted to the coronary care unit of Newham General Hospital with acute coronary syndromes. Repeat admissions during this period (n = 66) were excluded, as were an additional 23 unstable angina patients who did not fulfill criteria for Braunwald class 3B: cardiac chest pain at rest within the preceding 48 h that was not attributable to noncardiac causes (10). This left 1,111 patients with a discharge diagnosis of myocardial infarction (n = 633) and Braunwald class 3B unstable angina (n = 478). Myocardial infarction was diagnosed if any two of the following three criteria were fulfilled: a) cardiac chest pain lasting at least 30 min; b) ≥0.1 mV ST elevation in at least one standard lead or ≥0.2 mV ST elevation in two or more contiguous chest leads, and c) creatine kinase ≥400 IU/liter (upper limit of reference range: 200 IU/liter).

Data collection.   Baseline clinical characteristics including demographic, clinical and biochemical data were collected prospectively by a dedicated cardiologist and stored on a purpose built electronic database. Aspirin and beta-adrenergic blocking agent therapy at the time of admission was recorded, as were previous hospital admissions with acute coronary syndromes and revascularization procedures (percutaneous transluminal coronary angioplasty and coronary artery bypass grafting [CABG]). Diabetes was recorded in patients on insulin, oral hypoglycemic drugs or dietary restriction. Hypertension was recorded in patients taking antihypertensive drugs. Current smokers were classified as smokers, while ex-smokers and nonsmokers were grouped as nonsmokers for the purpose of this study. If racial group (African, Asian, white) was not obvious, it was determined by direct inquiry. Blood samples were taken in the Emergency Department for measurement of cholesterol, glucose, potassium and creatinine concentrations. The upper limit of the reference range for creatinine in our laboratory is 106 µmol/liter.

Statistical analysis.   Comparison of discrete variables was by chi-square analysis and continuous variables by the Mann–Whitney U test. To evaluate their independent influence, variables showing significant differences or marked trends in univariate analyses or believed to be of clinical or biological relevance were entered into a logistic regression analysis for which there were 1,008 complete data sets, representing 90.7% of all patients included in the study. Improvements in model fit were based on comparison of likelihood ratios. Odds ratios are quoted together with 95% confidence intervals.


   Results
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Discussion
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Clinical characteristics.   Table 1 shows baseline clinical characteristics of patients with acute myocardial infarction and unstable angina. There were small differences in the age and gender distributions between the groups, patients with myocardial infarction being older and more commonly male, but the groups were similar as regards racial groups. Significantly fewer patients with myocardial infarction than unstable angina were on treatment with aspirin and beta-blockers at the time of admission, but more were smokers. Hypertension, previous coronary syndromes and previous myocardial revascularization procedures were all less common in patients with myocardial infarction.


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  		Table 1 Baseline Characteristics

 
Admission biochemistry.   Although diabetes was somewhat less common in patients with myocardial infarction, their admission blood glucose concentration tended to be higher and potassium tended to be lower compared with patients with unstable angina. Blood creatinine concentration tended to be higher in patients with myocardial infarction. Cholesterol concentrations showed no difference between the groups (Table 2).


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  		Table 2 Admission Biochemistry

 
Multivariate predictors of discharge diagnosis.   Stratification by age showed that in patients >70 years the odds of myocardial infarction were more than double those of unstable angina. Smoking increased the odds of infarction by almost half. In patients admitted on aspirin, the odds of infarction were about one third, and in patients with a history of hypertension about two thirds those of unstable angina. Previous acute coronary syndromes and revascularization procedures each reduced the odds of infarction by about two thirds. Among biochemical variables, an increase in creatinine from the 10th (80 µmol/liter) to the 90th (140 mmol/liter) centile of the distribution increased the odds of myocardial infarction by one third relative to unstable angina (Table 3).


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  		Table 3 Multivariate Predictors of Discharge Diagnosis

 
Predictors of Non–Q wave myocardial infarction.   Non–Q wave infarction was recorded in 217 of the patients with a discharge diagnosis of myocardial infarction. Analysis of those variables applied in Table 3 showed that the only significant multivariate predictor of non–Q wave infarction was hypertension (odds ratio 1.64; 95% confidence interval 1.10 to 2.45).


   Discussion
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This prospective cohort study of patients with acute coronary syndromes has shown that the mode of presentation may be influenced by a range of clinical, therapeutic and biochemical factors. Many of these factors have the capacity to interact with the hemostatic system and modify thrombotic responses to plaque rupture, prothrombotic effects favoring coronary occlusion and myocardial infarction, antithrombotic effects favoring coronary patency and unstable angina. Other factors may modify the ischemic consequences of plaque events by affecting myocardial mass and the collateralization of the coronary circulation.

The effect of aspirin.   Our finding that patients with acute coronary syndromes who were taking aspirin were more likely to be discharged with a diagnosis of unstable angina than myocardial infarction confirms the observations of Garcio-Dorado et al. (9) and is presumably attributable to the effects of aspirin on the thrombotic process. Aspirin inhibits thromboxane synthesis, which in turn inhibits platelet aggregation and thrombus formation. It is possible to speculate, therefore, that reduction of the thrombotic response to plaque rupture in those patients taking aspirin helped preserve coronary patency and resulted in proportionately more of them developing unstable angina. If the clinical expression of plaque events can be modified in this way, it is also possible to speculate that an indeterminate number of patients treated with aspirin who would otherwise have an ischemic event may experience no symptoms at all if thrombus formation is diminished to the point that it remains confined within the plaque without affecting coronary flow. Subclinical plaque rupture of this type is found at autopsy in up to 5% of individuals who have coronary atheroma but die of noncardiac causes (11). The potential for aspirin to influence the pathogenesis of plaque events in this way may contribute importantly to its prognostic benefits in patients with coronary artery disease.

The effect of smoking.   If the antithrombotic effects of aspirin help preserve coronary patency following plaque rupture, favoring presentation with unstable angina, then prothrombotic factors would be expected to exaggerate the thrombotic response and heighten the probability of coronary occlusion and myocardial infarction. This may explain why current smokers were more likely to be discharged with a diagnosis of myocardial infarction than unstable angina. The prothombotic effects of smoking are well documented and include increased circulating levels of fibrinogen and adverse effects on coronary endothelial function with platelet activation and alterations in the secretion of tissue plasminogen activator and its inhibitor (PAI-1), which combine to reduce fibrinolytic activity (12–14). Moreover endothelium-dependent vasodilatation is compromised in smokers, reducing coronary luminal diameter and heightening still further the probability of coronary occlusion for a given thrombotic response (15). Thus the adverse prognostic effects of smoking may relate not only to the increased risk of developing atherosclerosis but also to the increased risk of occlusive thrombosis and myocardial infarction. Indeed, in young patients, cigarette smoking has been associated with thrombotic coronary occlusion even in the absence of angiographic atherosclerotic disease (16).

Other prothrombotic factors: age and renal impairment.   The effect of advanced age on the mode of presentation was similar to that of smoking, patients >70 years being over twice as likely to have a discharge diagnosis of myocardial infarction than unstable angina. Again, a plausible explanation for this finding is age-related changes in vascular endothelial function (17,18) and thrombogenicity, the elderly showing marked increases in circulating fibrinogen and factor VII levels compared with younger individuals (19). Age-related deterioration in renal function may also contribute to enhanced thrombogenicity in the elderly through deleterious effects on endothelial function with adverse consequences for fibrinolytic activity and coronary vasodilator responses (20–23). Indeed our data suggest an independent effect of renal function, an increase in creatinine from the 10th (80 µmol/liter) to the 90th (140 mmol/liter) centile of the distribution increasing the odds of myocardial infarction by nearly one third. Other differences in biochemical variables included a tendency for blood glucose to be higher and potassium lower in the infarct groups, probably reflecting greater sympathoadrenal activation in myocardial infarction, which stimulates glycogenolysis and drives potassium intracellularly (24,25).

Left ventricular hypertrophy and coronary collaterals.   Other factors apart from enhanced thrombogenicity may play a contributory role in determining the clinical expression of plaque events. In hypertension, for example, endothelial dysfunction is common (26,27), but our data suggest that any associated tendency toward increased thrombogenicity and myocardial infarction is outweighed by the increased oxygen demand of the hypertrophied ventricle, which ensures that some plaque events that would normally be silent provoke presentation with unstable angina. Endothelial function may also be impaired in diabetes (28–30), yet this did not appear to affect the mode of presentation. This was surprising but may reflect other differences between diabetic and nondiabetic coronary artery disease combining to obscure those attributable to enhanced thrombogenicity. One possibility is that the diffuse and chronic nature of diabetic coronary disease (31) encourages collateralization of the myocardium, which protects against ischemic injury in the event of thrombotic coronary occlusion (32,33). This may also account for the independent effect of previous coronary syndromes and revascularization procedures, which each favored presentation with unstable angina, reducing the odds of infarction by about two thirds.

Non–Q wave myocardial infarction.   Previous investigators have reported that aspirin consumption may also modify the presentation of acute myocardial infarction by protecting against Q wave development (9,34,35). We were unable to confirm this in our patient population, possibly because the inner-city location of our hospital ensure that patients with myocardial infarction present early, and the majority (>70%) are eligible for thrombolytic therapy, obscuring the potential influence of prior aspirin therapy on Q wave development (36). Indeed the only multivariate predictor of non–Q wave infarction was hypertension, presumably reflecting the vulnerability of the hypertrophied ventricle to subendocardial ischemic damage.

Conclusions.   A range of factors with the capacity to influence thrombogenicity, myocardial mass and collateralization of the coronary circulation may also influence the clinical presentation of patients with acute coronary syndromes. Our data show that presentation with myocardial infarction is favored by cigarette smoking, advanced age and renal impairment, all of which increase thrombogenicity. Presentation with unstable angina is favored by treatment with aspirin, which reduces thrombogenicity, hypertension, which increases myocardial mass and a history of previous coronary syndromes and revascularization procedures, which may be associated with increased collateralization of the coronary circulation.


   References
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 Abstract
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 References
 

  1. Davies MJ, Thomas AC. Plaque fissuring: the cause of acute myocardial infarction, sudden ischaemic death, and crescendo angina. Br Heart J. 1983;50:127–134[Abstract/Free Full Text]
  2. Fuster V, Badimon L, Badimon JJ, Chesebro JH. The pathogenesis of coronary artery disease and the acute coronary syndromes (part 1). N Engl J Med. 1992;326:242–250[Medline]
  3. Fuster V, Badimon L, Badimon JJ, Chesebro JH. The pathogenesis of coronary artery disease and the acute coronary syndromes (part 2). N Engl J Med. 1992;326:310–318[Medline]
  4. Davies MJ. Acute coronary thrombosis—the role of plaque disruption and its initiation and prevention. Eur Heart J. 1995;16(Suppl L):3–7[Medline]
  5. Celermajer DS. Endothelial dysfunction: does it matter? Is it reversible? J Am Coll Cardiol. 1997;30:325–333[Abstract]
  6. Gusto Angiographic Investigators. The effects of tissue plasminogen activator, streptokinase, or both on coronary artery patency, ventricular function, and survival after acute myocardial infarction. N Engl J Med. 1993;329:1615–1622[Abstract/Free Full Text]
  7. Oler A, Wholey MA, Older J, et al. Adding heparin to aspirin reduces the incidence of myocardial infarction and death in patients with unstable angina. A meta-analysis. JAMA. 1996;276:811–815[Abstract]
  8. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Indications for firinolytic therapy in suspected myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Lancet. 1994;343:311–322[CrossRef][Medline]
  9. Garcia-Dorado D, Theroux P, Tornos P, et al. Previous aspirin use may attenuate the severity of the manifestation of acute ischemic syndromes. Circulation. 1995;92:1743–1748[Abstract/Free Full Text]
  10. Braunwald E. Unstable angina: a classification. Circulation. 1989;80:410–414[Free Full Text]
  11. Davies M, Bland J, Hangartner J, Angelini A, Thomas A. Factors influencing the presence or absence of acute coronary artery thrombi in sudden ischaemic death. Eur Heart J. 1989;10:203–208[Abstract/Free Full Text]
  12. Blache D. Involvement of hydrogen and lipid peroxides in acute tobacco-induced platelet hyperactivity. Am J Physiol. 1995;268:679–685
  13. Lowe GDO, Fowkes FGR, Dawes J, Donnan PT, Lennie ST, Housley E. Blood viscosity, fibrinogen and activation of coagulation and leucocytes in peripheral arterial disease and the normal population in the Edinburgh Artery Study. Circulation. 1993;87:1915–1920[Abstract/Free Full Text]
  14. Simpson AJ, Gray RS, Moore NR, Booth NA. The effects of chronic smoking on the fibrinolytic potential of plasma and platelets. Br J Haematol. 1997;97:208–213[CrossRef][Medline]
  15. Celermajer DS, Sorensen KE, Georgakopoulos D, et al. Cigarette smoking is associated with dose related and potentially reversible impairment of endothelial-dependent arterial dilation in healthy young adults. N Engl J Med. 1996;334:150–154[Abstract/Free Full Text]
  16. Brecker SJD, Stevenson RN, Roberts R, Uthayakumar S, Timmis AD, Balcon R. Acute myocardial infarction in patients with normal coronary arteries. Br Med J. 1993;307:1255–1256[Medline]
  17. Zeiher AM, Drexler H, Saurbier B, Just H. Endothelium-mediated coronary blood flow modulation in humans: effects of age, atherosclerosis, hypercholesterolemia, and hypertension. J Clin Invest. 1993;92:652–662[Medline]
  18. Barton M, Cosentino F, Brandes RP, Moreau P, Shaw S, Lüscher TF. Anatomical heterogeneity of vascular aging: role of nitric oxide and endothelin. Hypertension. 1997;30:817–824[Abstract/Free Full Text]
  19. Lowe GDO, Rumley A, Woodward M, et al. Epidemiology of coagulation factors, inhibitors and activation markers: the Third Glasgow MONICA Survey. Br J Haematol. 1997;97:775–784[CrossRef][Medline]
  20. Haaber AB, Eidemake I, Jensen T, Feldt-Rasmusen B, Strangaard S. Vascular endothelial cell function and cardiovascular risk factors in patients with chronic renal failure. J Am Soc Nephrol. 1995;5:1581–1584[Abstract]
  21. Gris JC, Branger B, Vecina F, al Sabadina B, Fourcade J, Schved JF. Increased cardiovascular risk factors and features of endothelial activation and dysfunction in dialysed uraemic patients. Kidney Int. 1994;46:807–813[Medline]
  22. Vallance P, Leone A, Calver A, Collier J, Moncada S. Accumulation of endogenous inhibitor of nitric oxide synthesis in chronic renal failure. Lancet. 1992;339:572–575[CrossRef][Medline]
  23. Ishii Y, Yano S, Kanai H, et al. Evaluation of blood coagulation-fibrinolysis system in patients receiving chronic haemodialysis. Nephron. 1996;73:407–412[Medline]
  24. Nordrehaug JE, Johannessen K-A, Von der Lippe G, Sederholm M, Grottum P, Kjekshus J. Effect of timolol on changes in serum potassium concentration during acute myocardial infarction. Br Heart J. 1985;53:388–393[Abstract/Free Full Text]
  25. Oswald GA, Smith CCT, Betteridge DJ, Yudkin JS. Determinants and importance of stress hyperglycaemia in non-diabetic patients with myocardial infarction. BMJ. 1986;293:917–922[Medline]
  26. Nava E, Noll G, Lüscher TF. Increased cardiac activity of nitric oxide synthase in spontaneous hypertension. Circulation. 1995;91:179–181
  27. Taddei S, Virdis A, Mattei P, Salvetti A. Vasodilation to acetylcholine in primary and secondary forms of human hypertension. Hypertension. 1993;21:929–933[Abstract/Free Full Text]
  28. Aronson D, Rayfield EJ, Chesebro JH. Mechanisms determining course and outcome of diabetic patients who have had acute myocardial infarction. Ann Intern Med. 1997;126:296–306[Abstract/Free Full Text]
  29. McGill JB, Schneider DJ, Arfken CL, et al. Factors responsible for impaired fibrinolysis in obese subjects and NIDDM patients. Diabetes. 1994;43:104–109[Abstract]
  30. Wincour PD. Platelet abnormalities in diabetes mellitus. Diabetes Metab Rev. 1992;8:53–56[Medline]
  31. Stone PH, Muller JE, Hartwell T, et al. The effect of diabetes mellitus on prognosis and serial left ventricular function after acute myocardial infarction: contribution of both coronary disease and diastolic left ventricular dysfunction to the adverse prognosis. J Am Coll Cardiol. 1989;14:49–57[Abstract]
  32. Habib GB, Heibig J, Forman SA, et al. Influence of collateral vessels on myocardial infarct size in humans: results of phase 1 Thrombolysis in Myocardial Infarction (TIMI) trial. Circulation. 1991;83:739–746[Abstract/Free Full Text]
  33. Cohen M, Sherman W, Rentrop KP, Gorlin R. Determinants of collateral filling observed during sudden controlled coronary artery occlusion in human subjects. J Am Coll Cardiol. 1989;13:297–303[Abstract]
  34. Col NF, Yarzebski J, Gore JM, Alpert JS, Goldberg RJ. Does aspirin consumption affect the presentation or severity of acute myocardial infarction? Arch Intern Med. 1995;155:1386–1389[Abstract]
  35. Lloyd-Jones DM, Camargo CA, Lapuerta P, Guigliano RP, O’Donnell CJ. Electrocardiographic and clinical predictors of acute myocardial infarction in patients with unstable angina pectoris. Am J Cardiol. 1998;81:1182–1186[CrossRef][Medline]
  36. Stevenson R, Ranjadayalan K, Wilkinson P, Roberts R, Timmis AD. Short and long term prognosis of acute myocardial infarction since introduction of thrombolysis. Br Med J. 1993;307:349–353[Medline]



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