Cardiovascular Disease: Acute Coronary Syndrome in Women Essay

Introduction

Coronary heart disease (CHD) is a major health problem that influences the quality of life and is a major threat to life as nearly 47% of individuals who suffer an acute coronary event will die from it. CHD is not a single disease; it includes acute and chronic ischaemic heart disease, angina pectoris, acute myocardial infarction, and atherosclerotic cardiovascular disease (AHA, 2002). The aim of this essay is to critically study a case of a female case of acute coronary syndrome, the path of discussion will focus on risk factors, pathogenesis and the role of emergency and CCU nurses.

Gender-Related Differences in Coronary Heart Disease

Cardiovascular disease is common in both genders, yet only recently, reported gender-related differences in epidemiology became perceptible. The WHO (MONICA project) in the late 1990s pointed that rate of coronary events are higher in males, and coronary heart disease (CHD) rates decreased more than disease fatality rates in both genders (Tunstall-Pedoe and others, 1999). In 2004, Arciero and colleagues showed that the prevalence of females presenting with clinical or angiographic evidence of CHD is increasing. Further, the reported rates of decline in incidence show it is true for males; however, in females the incidence rate is stable over the past 20 years. The American Heart Association (2002) pointed that the prevalence of cardiovascular disease in young age groups is lower in females, yet, it increases with age, and the gender gap narrows significantly with age.

Cardiovascular disease is the leading cause of death in females where it is responsible for one-third of female deaths worldwide. The gender differences are not only in epidemiology; as the disease affects both genders differently, for example females with diabetes have higher cardiovascular mortality rates than males. Besides, CHD incidence in females increases nearly threefold after menopause (AHA, 2002). Further, there are many factors that influence the gender difference in prevalence, which include cultural, behavioural, psychosocial and socioeconomic factors. In addition, females were under represented in most epidemiological gap, which has created a knowledge gap that might explain why females’ cardiovascular prevalence is not improving as it is for men (Rabi and Cox, 2007).

Risk Factors of Coronary Heart Disease

Recognizing risk factors is essential because if treated, managed or reduced, a significant decrease in disease prevalence and morbidity results (Hu et al, 2000). Epidemiological research identified four major risk factors namely diabetes, hypertension, hyperlipidaemia and cigarette smoking. The importance of these factors is because they are independent and evidence shows controlling these factors significantly reduces CHD morbidity (Khot et al, 2003). However, it is a common inference that in nearly 50% of CHD cases, none of these four conventional risk factors is present. This led to significant research for other risk factors (Robinson and Loscalzo, 2002). Recent evidence shows that physical inactivity and obesity as lifestyle factors are important risk factors (Castanho et al, 2001). In addition, genetic factors are blamed as risk factors to CHD (Nabel, 2003). In the context of the case presented (see appendix), the discussion on risk factors will focus on diabetes and hypertension.

Diabetes as a Risk Factor of Coronary Heart Disease

Coronary heart disease disproportionately affects diabetic patients, further despite the advances made in the understanding of CHD risk factors and management; yet, diabetic patients again disproportionately benefited from them. This is because of the association of other risk factors present in this group of patient like dyslipidaemia, obesity, hypertension and the association of other non-traditional risk factors (Fonseca, 2000). The Atherosclerosis Risk in Communities (ARIC) study report (2004) points to the risk of CHD in diabetic patients related to non-traditional risk factors, mainly high levels of albumin, von Willebrand, fibrinogen, factor VIII. Other risk factors reported were increased levels of high-density lipoproteins, cholesterol and apolipoproteins, of these factors the first four are independent (ARIC report, 2004).

Huerta and Nadler (2002, p.396) explained that these risk factors reflect a non-specific inflammatory process possibly secondary to atherosclerosis, or increase the possibility of coagulation and thrombotic process, which brings about a vascular event. In 2007, data from the American Heart Association showed that the increased incidence of diabetes is associated with increased prevalence of cardiovascular disease; moreover, the report suggests that increasing rates of diabetes threaten the trend of lowering CHD events. Further, the report showed that diabetic females are less investigated than are male counterpart for non-traditional risk factors (Rosamond et al, 2007).

Hypertension as a Risk Factor for Coronary Heart Disease

Hypertensive patients are at more risk to develop cardiovascular disease than normotensive individuals are, it is an important risk factor to consider because of its high frequency an impact on cardiovascular and kidney disease and the fact of being a modifiable risk factor. The high prevalence of hypertension contributed to the present wide prevalence of cardiovascular disease (Kearney et al, 2005). Control of hypertension is important in reducing cardiovascular disease morbidity and mortality in many large prospective randomized clinical trials (Rosamond et al, 2007). The question is mild hypertension a risk factor to CVD, Vasan and colleagues (2001, p.1291) showed that high normal blood pressure is a risk factor of CVD. The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JCN) defined individuals with blood pressure of 120-139/80-89 as pre-hypertensive patients (Hsia et al, 2007). Many research studies confirmed pre-hypertension as a risk factor of CHD and myocardial infarction (Qureshi et al, 2005). Wang and colleagues (2006, p. 403) showed the pre-hypertensive patients have nearly double the risk of developing cardiovascular disease, and age and diabetes are significant independent factors to cardiovascular disease risk. Hsia et al (2007, p. 855) suggested that pre-hypertension notably links to increased risk of cardiovascular disease in postmenopausal females.

Pathogenesis of Coronary Heart Disease

The definition of acute coronary syndrome includes all clinical conditions of myocardial ischaemia manifested by chest pain or discomfort, which appears suddenly at rest or accompanying minimal effort. Chest pain may be typical, atypical or accompanied by other symptoms as dyspnoea. Typically, chest pain occurs in patients who have coronary atherosclerosis and links to rupture or erosion of a susceptible plaque (Mittal, 2005).

The balance between coronary blood flow and coronary vessel resistance determines myocardial blood supply. Stable (typical or exertion) angina occurs when the flow in one or more coronary artery is significantly reduced because of stenosis mainly secondary to atherosclerotic coronary artery disease. With effort or emotional stress the oxygen requirements of the cardiac muscle increase, that should be met with dilatation of the coronary arteries providing more oxygenated blood. If this fails because of coronary stenosis, the balance between myocardial demand and oxygen supply is disturbed producing ischaemia, which develops mainly in the inner part of the heart muscle wall. Besides pain, ischaemia causes decline in creatine phosphate and ATP (myocardial cells’ high-energy phosphates), as a result, ventricular contractility and diastolic relaxation in the area affected are impaired. The result is reduced cardiac output with the consequent symptoms of dyspnea (pulmonary congestion) and anxiety (sympathetic activation). Infarction is tissue death secondary to severe ischaemia and it occurs where an area of localized ischaemia causes a defined area of cell death (necrosis) with succeeding inflammation and scarring. Myocardial infarction is commonly caused by rupture of an atheromatous plaque exposing a rough endothelial surface that predisposes to thrombosis and further coronary artery occlusion (Aaronson and Ward, 2007).

Case Study Summary

A 58-year-old female arrives at the emergency department complaining of chest discomfort.

The discomfort began 1 hour ago, during breakfast, and described this discomfort as dull and pressure-like. She has some mild central chest discomfort, with radiation to her left arm and left jaw. She feels slightly short of breath.

The patient has diabetes and hypertension and takes hydrochlorothiazide and glyburide. Her blood pressure is 150/100 mmHg, pulse rate is 95 bpm and regular, respirations are 22 breaths per minute, temperature 37.3’C, and oxygen saturation by pulse oximetry is 98 per cent on room air.

The patient is diaphoretic and appears anxious. On auscultation, faint crackles are heard at both lung bases. The cardiac exam reveals an S3 gallop and is otherwise normal. On examination, she has no other abnormalities.

She has had no other cardiac events. The ECG shows a configuration of acute myocardial infarction. ST-segment elevation in Leads II, III, AVF, reciprocal changes in lead I and AVL ST depression and T wave Inversion which means ischemic changes. There is also ST depression and T wave inversion in Lead V1, V2, V3, and V4.

Case Study: Interpretation of Clinical Manifestations

The mainstay in acute coronary syndrome (ACS) management is to recognize the short period to make a diagnosis with speed, promptness and efficiency to establish reperfusion to improve ventricular dysfunction and consequently survival. Diagnosis depends on interpreting the clinical presentation, electrocardiograms and results of cardiac muscle injury biomarkers. Clinical presentation is significant being the first chance to build a correct diagnosis or at least a high suspicion index (Bavry et al, 2006). Chest pain is a cardinal symptom that is usually described as retrosternal pain, heaviness or discomfort, it may present on the left side of the chest wall, left shoulder, arm, back, neck or jaw. This diversity in location may misdirect diagnosis to other considerations like dissecting aortic aneurysm or pulmonary embolism (Milner et al, 2004). Cases of ACS may be silent (no chest pain), or patients may give vague symptoms, which are common in elderly and diabetic patients. In these cases, attention should be directed to accompanying symptoms of diaphoresis, dyspnea and nausea, (Bugiardini et al, 2005).

Brieger et al (2004, p. 461) performed a multivariate analysis to determine the relevance of diaphoresis, dyspnoea, nausea or vomiting and syncope or pre syncope. There results suggested the dominance of dyspnoea followed by diaphoresis nausea and pre syncope or syncope. In this context, the association of diaphoresis, chest pain and dyspnoea increases risk possibilities for this particular patient. Females with ACS are less likely to report chest pain or tend to reduce its severity. Despite differences are not significant to affirm a general judgment; yet, it must be considered when dealing with a female case (Canto et al, 2007). Arsalanian and colleagues (2006, p. 1177) compared symptoms of males and females with ACS and inferred that men more commonly present with chest pain and diaphoresis while females present more commonly with nausea, while dyspnea did not differ in both groups. They also inferred that diaphoresis and nausea are important risk predictors in both genders.

The third sound S3 coincides with early diastolic left ventricle filling, despite normally heard in young adults, yet in the case at hand, it is indicative of heart failure. Gallop or triple rhythms is an important sign of heart failure per se irrespective of the cause and indicate cardiac muscle damage. Further, fine basal crepitations (crackles) are early sign of left ventricular heart failure and the intensity of crepitations parallels the degree of dyspnea. It should always be remembered that congestive heart failure might be the first manifestation of coronary artery disease among the diabetic population (Habermann and Ghosh, 2008).

Drug-drug interaction between hydrochlorothiazide (a diuretic used in the treatment of hypertension) and glyburide (a member of sulfonylurea hypoglycaemic agents) exist. Hydrochlorothiazide increases blood glucose level counteracting glyburide effect, in clinical terms, this means unsuccessful management of this patient’s risk factors (Ogbru and Marks, 2009). At this stage, the provisional diagnosis is acute coronary syndrome with early acute heart failure. This patient is at high risk having ongoing chest pain lasting for more than 20 minutes, diaphoresis, slow pulse rate (indicative of pre syncope) and dyspnoea (ICSI healthcare guidelines, 2008).

Case Study: Interpretation of Electrocardiogram

ECG is a key diagnostic test in this case; besides being available and quick to perform, it provides significant information that helps to risk stratify patients. It is a rapid method to triage patient usually to ST elevation or non-ST elevation ACS, thus, it helps to recognize patients who are in need for rapid reperfusion therapy (de Luna and Fiol-Sala, 2008). Changes in ST segment of an ECG represent ventricular re-polarization, and record in the area of myocardial sub-endocardium or sub-epicardium diastolic depolarization because of significant decrease in blood supply (ischemia or infarction). The leads facing the injured (infarct area) show ST depression when injury is dominant in the sub-endocardium, and ST elevation if the injury is sub-epicardial (sub-endocardial and sub-epicardial injury patterns respectively). ST-segment elevation of 2 cm or more in leads V1 to V3 and of 1 cm or more in other leads is indicative of a myocardial infarction. Elevated ST segment in V1 is the criterion of highest accuracy in predicting an infarct (Camm et al, 2006). Sub-endocardial ischaemia typically results in depressed ST segment and T-wave inversion. Trans-mural ischaemia results in ST elevation with vector shift to the involved epicardial layer (de Luna and Fiol-Sala, 2008).

Reciprocal ST segment depression occurs in leads that are electrically opposite to the injured area. The presence of reciprocal changes is a highly sensitive indicator of myocardial infarction and occurs in 70% of cases of inferior infarction and in 30% of anterior infarction cases. Further, their presence is helpful where there is doubt about the significance of ST-segment elevation; they strongly indicate infarction with estimated 90% sensitivity (Morris and Brady, 2002). The ECG shows a range of risk stratification in which combined ST elevation and depression represent the highest risk, isolated small T-wave inversion is at the lower risk range and ST depression alone is at the intermediate risk range (de Luna and Fiol-Sala, 2008).

T-wave is normally upright in leads I, II and V3 to V6 (left-sided leads) and inverted in leads III, aVF and aVL. Abnormally inverted T-wave in the presence of acute coronary syndrome symptoms is indicative of ischaemia, Further, T-wave inversion with ST change may point to transient ischaemia or spontaneous reperfusion, however with significant ST changes it points to myocardial injury (Smith and Whitwam, 2006).

With the ECG description at hand (see appendix), elevated ST segment points to inferior myocardial infarction. ST segment depression in the anterior leads V1 to V4 points to myocardial ischaemia when combined with T-wave inversion in the same leads indicate inferior infarction and opposite wall ischaemia. Reciprocal changes in leads I and aVL, strongly indicate inferior infarction.

Diagnosis From a Nursing Perspective

The North American Nursing Association (NANDA) defines nursing diagnosis as a standardized statement about a client’s health for providing nursing care. According to the NANDA system, there are five pillars for a nursing diagnosis, which are the actual diagnosis or statement of the health problem, a risk problem that is the risk expected and the risk factors of the present condition. Third is the possible diagnosis, which is the diagnosis of possible health problem (s) that the patient might have already but the nurse has no information about it yet. Fourth are the syndrome diagnosis when the patient has multiple diagnoses together, and finally, the wellness diagnosis, which describes the expected outcome. Since the NADA’s list of diagnoses has increased, PES format, which joins the five, pillars structure into, Problem, Aetiology, Signs and symptoms (Doenges and Moorhouse, 2003). Based on the above discussion a nursing diagnosis for the case at hand would be: High-risk inferior myocardial infarction with ischaemia, uncontrolled hypertension, needs further assessment for diabetes. Deficient knowledge cardiac biomarkers (enzymes), eminent syncope, manifested by sweating, anxiety, slow for case heart rate, and may need rapid reperfusion therapy.

Further Management (What to Do and What is Next)

Immediate management of acute coronary syndrome has two interconnecting objectives. First is to address the current problem and second is to prevent complications and achieve stabilization (Libby and Theroux, 2005). In this context, a blood sample for cardiac injury biomarkers (cardiac enzyme) should be taken and sent to the lab. However if diagnosis is established, waiting for results of cardiac biomarkers in ST elevation myocardial infarction (the case at hand) to start effective management is risky to the patient and is therefore contraindicated (Bavry and Bahtt, 2009). Second is to work on relieving the patient’s pain, anxiety and dyspnea, with continuous monitoring of the patient to detect complication until transference to coronary care unit. The question of starting intervention whether percutaneous coronary interventions, antifibrinolytic or antithrombotic treatment is subject to discussions (Van de Werf et al, 2008). Decision making for reperfusion or antifibrinolytic treatment in emergency room depends on many variables. These are time elapsed since the onset of symptoms, risk stratification of the case, risk of treatment (concurrent injury, treatment or medical condition), and the time needed to transfer the patient to CCU with the feasibility of percutaneous coronary intervention. Within the range of three hours from the onset, there is no danger and no preference between the two modalities. Absolute contraindications for fibrinolytic treatment in ER are past history of intracranial haemorrhage, intracranial malignant neoplasm (primary or secondary), and history of known cerebral vascular abnormality. Other absolute contraindications include past history of significant closed head trauma during the past three months, bleeding or history of a bleeding disorder, and ischaemic stroke during the past three months (except recent acute stroke during the past three hours) (Van de Werf et al, 2008).

Role of Emergency Nurse

The first duty of an emergency room nurse after acknowledging the patient’s symptoms and signs is to take a brief and targeted history then to triage the patient for placement in an acute area of the emergency department. A 12-leads ECG should be done with 10 minutes from arrival to ER. In the acute area, the emergency nurse should put the patient to a cardiac monitor, take a blood sample for blood studies (including biomarkers), oxygen therapy, and be ready with and for nitroglycerin-aspirin preliminary treatment and further intervention. The nursing staff should do this supervised by the nurse in charge while the emergency physician is attending the patient and interpreting the CCG. The nurse in charge should administer other medications as ordered by the emergency physician like morphine, nitrates, and or beta-blockers. A contact should be made with the CCU for quick patient transfer to continue the management per protocol (ACC, 2004).

Role of CCU Nurse

The primary management objective in the coronary care unit (CCU) is balancing maximization of cardiac output and minimizing cardiac workload. This case study patient should have frequent vital signs measurements; continue on a cardiac monitoring specifically monitoring the ST segment changes. The leads selected for monitoring are based on the site of infarction taking in consideration the cardiac rhythm, with frequent serial ECGS taken for evaluation and follow-up. Collection of blood tests especially serum cardiac enzymes; serum chemistry and blood tests with serial evaluation of the levels of cardiac enzymes and blood glucose. Monitoring pulse oximetry for early detection of hypoxaemia and attention to chest pain taking in consideration, the nitrates do not substitute analgesics. The nurse in charge should be aware that first 12 hours of admission are important to achieve haemodynamic stability and chest pain relief; therefore, bed rest, restriction of physical activity and keeping commodities at bedside are helpful measures. At this early stage of admission to the CCU, patients like the one at hand are often given nothing by mouth until pain relief, when the conditions become stable they start clear fluids and move to heart-healthy food considering the diabetic state. Further, straining as with Valsalva’s manoeuvre is not encouraged as it affects cardiac rhythm and increases systolic pressure accordingly increasing the cardiac workload, stools softeners not laxatives are advised to avoid straining. The nurse in charge should record the patient’s daily weight to detect fluid retention. Thus, the CCU nurse priorities at this stage are relief of chest pain and anxiety, reducing cardiac workload, and preventing, detecting, and assisting in the management of complications when arise. Examples of nursing diagnoses at this stage are (activity intolerance related to decreased cardiac output or alterations in myocardial tissue perfusion), and (persistent chest pain related to myocardial infarction, decreased cardiac output with ECG changes showing…). The nurse staff should remain in contact with the CCU resident notifying him with updated changes as they occur, at the same time a CCU nurse should complete the nursing admission database (Doenges et al, 2008).

Conclusion

Coronary artery syndrome including myocardial infarction links strongly to a number of modifiable risk factors. Assessment in emergency room is helpful in reaching a quick diagnosis and in risk stratification; thus it is a key to an immediate successful management. This influences prognosis and late outcomes of the myocardial infarction incident. The emergency nurse plays a pivotal role in diagnosis, risk stratification and management. The CCU nurse is a central member of the team who is responsible for reviewing the patient’s data in continuum and analysing successes or failures at any point of the process.

References

1. Aaronson, P. I., and Ward, J. P. (2007). The Cardiovascular System at a Glance. Malden, Ma: Wiley-Blackwell.
2. Arciero, T.J., Jacobson, S.L., Reeder, G.S., et al (2004). Temporal trends in the incidence of coronary disease. Am J Med, 117, 228-233.
3. ACC (American College of Cardiology). (2004). Management of Patients with ST-Elevation Myocardial infarction. Washington DC: Author.
4. American Heart Association (AHA). (2002). Heart Diseases and Stroke Statistics-2003 Update. Dallas, Tex: American Heart Association.
5. Atherosclerosis Risk in Communities (ARIC). (2006). Community Surveillance and Cohort Morbidity/Mortality Follow-Up. Chapel Hill, NC: Department of Biostatistics, University of North Carolina.
6. Brieger, D., Eagle, K. A., Goodman, S. G., et al (2004). Acute Coronary Syndromes without Chest Pain, an Underdiagnosed and Untreated High-Risk Group: Insights from the Global Registry of Acute Coronary Events. Chest, 126, 461-469.
7. Bavry, A.A., Kumbhani, D.J., Rassi, A.N., et al. (2006). Benefit of early invasive therapy in acute coronary syndromes: a meta-analysis of contemporary randomized clinical trials. J Am Coll Cardiol, 48, 1319–1325.
8. Bavry, A., A., and Bhatt, D. L. (2009). Acute Coronary Syndromes in Clinical Practice. London: Springer-Verlag.
9. Bugiardini, R., Bairey Merz, C. N. (2005). Angina with “normal” coronary arteries: a changing philosophy. JAMA, 239, 477-484.
10. Camm, A. J., Luscher, T. F., and Serruys, P. W. (2006). The ESC Textbook of Cardiovascular Medicine. Oxford, UK: Blackwell Publishing.
11. Canto, J. G., Goldberg, R. J., Hand, M. M., et al (2007). Symptom Presentation of Women With Acute Coronary Syndromes: Myths vs Reality. Arch Intern Med, 167(22), 2405-2413.
12. Castanho, V.S., Oliveira, L.S., Pinheiro, H.P. et al (2001). Sex differences in risk factors for coronary heart disease: a study in a Brazilian population. BMC Public Health, 1, 3-9.
13. de Luna, B., and Fiol-Sala, M. (2008). The Surface Electrocardiography in Ischaemic Heart Disease: Clinical and Imaging Correlations and Prognostic Implications. Malden, MA: Blackwell Futura.
14. Doenges, M. E., and Moorhouse, M. F. (2003). Application of Nursing Process and Nursing Diagnosis: An Interactive Text for Diagnostic Reasoning (4^th. Edition). Philadelphia: F.A. Davis Company
15. Doenges, M. E., Moorhouse, M. F., and Murr, A., C. (2008). Nursing Diagnosis Manual. Philadelphia: F.A.Davis Company.
16. Fonseca, V. A., (2000). Risk Factors for Coronary Heart Disease in Diabetes. Annals of Internal Medicine, 133(2), 154-156
17. Habermann, T. M., Ghosh, A. K. (2008). Mayo Clinic Internal Medicine Concise Textbook. Rochester, Mn: Mayo Clinic Scientific Press-Informa Healthcare.
18. Hsia, J., Margolis, K. L., Eaton, C. B., et al (2007). Prehypertension and Cardiovascular Disease Risk in the Women’s Health Initiative. Circulation, 115, 855-860.
19. Hu, F.B., Stampfer, M.J., Manson, J., et al (2000). Trends in incidence of coronary heart disease and changes in diet and lifestyle in women. N Engl J Med, 343, 530-537.
20. Huerta. M.G., Nadler, J.L., (2002). Role of inflammatory pathways in the development and cardiovascular complications of type 2 diabetes. Curr Diab Rep, 2, 396–402.
21. ICSI (Institute for Clinical Systems Improvement). (2008). Health Care Guideline: Diagnosis and Treatment of Chest Pain and Acute Coronary Syndrome (ACS). Bloomington, MN: Institute for Clinical Systems Improvement.
22. Kearney, P. M., Whelton, M., Reynolds, K. et al (2005). Global burden of hypertension: analysis of worldwide data. Lancet, 365, 217-223.
23. Khot, U.N., Khot, M.B., Bajzer, C.T., et al (2003). Prevalence of Conventional Risk Factors in Patients with Coronary Heart Disease. JAMA, 290(7), 898-904.
24. Libby, P., and Theroux, P. (2005). Pathophysiology of Coronary Artery Disease. Circulation, 111, 3841-3488.
25. Milner, K. A., Vaccarino, V., Arnold, A. L., et al (2004). Gender and age differences in chief complaints of acute myocardial infarction (Worcester Heart Attack Study). Am J Cardiol, 93, 606-608.
26. Mittal, S. (2005). Coronary Heart Disease in Clinical Practice. New York: Springer.
27. Morris, F., and Brady, W. J. (2002). ABC of clinical electrocardiography: Acute myocardial infarction: Part I. BMJ, 324, 831-834.
28. Nabel, E. (2003). Cardiovascular disease. N Engl J Med, 349, 60-72.
29. Ogbru, O., and Marks, J. W. (2009). Glyburide.
30. Qureshi, A. I., Fareed, M., Suri, K., et al (2005). Is Prehypertension a Risk Factor for Cardiovascular Diseases? Stroke, 36, 1859-1863.
31. Rabi, D., and Cox, J. (2007). Burden of cardiovascular disease in women and men. CMAJ, 176(6), S1-S44.
32. Robinson K., and Loscalzo, J. (2002). Other risk factors for coronary artery disease: homocysteine, lipoprotein (a), fibrinogen, and plasminogen activator factor. In: Topol E.J., ed. Textbook of Cardiovascular Medicine. Philadelphia, Pa: Lippincott Williams & Wilkins, P. 200.
33. Rosamond, W., Flegal, K., Friday, G., et al (2007). Heart Disease and Stroke Statistics-2007 Update: A Report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation, 115, e69-e171.
34. Smith, S.W., and Whitwam, W. (2006). Acute Coronary Syndromes. Emerg Med Clin N Am, 24, 53-89.
35. Tunstall-Pedoe, H., Kuulasmaa, K., Mahonem, M., et al (1999). Contribution of trends in survival and coronary event rates to changes in coronary heart disease mortality: 10-year results from 37 WHO MONICA project populations. Monitoring and determinants in cardiovascular diseases. Lancet, 353, 1547-1557.
36. Van der Werf, F., Bax, J., Betriu, A., et al. (2008). Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation. European Heart Journal, 29, 2909-2945.
37. Vasan, R. S., Larson, M. G., Leip, E. P., et al (2001). Impact High Blood Pressure on the Risk of Cardiovascular Disease. N Engl J Med, 345(18), 1291-1297.
38. Wang, W., Lee, E. T., Fabsitz, R. R., et al (2006). A Longitudinal Study of Hypertension Risk Factors and Their Relation to Cardiovascular Disease. Hypertension, 47, 403-409.