Evolution of Stable Angina into Acute Myocardial Infarction - Essay Example

 Evolution of Stable Angina into Acute Myocardial Infarction Introduction Stabile angina pectoris is a symptom that is associated with coronary vascular disease. It is a subjective feeling of chest pain, pressure, burning sensation or some other subjective feeling described by the patient that usually appears after physical exercise, intense emotional stimulus, stress or other provoking factor (Somerville et al. 2008). It is very variable symptom that varies when is described by different patients, and this makes it one of the most controversial symptoms in the medicine (Melvyn et al. 2010). Stabile angina pectoris is usually first recognized during a general practice (GP) doctor visit, or is noticed by a nurse during a home visit or other occasion. GP doctors often must decide if the acute symptoms described by the patient are due to heart problems or some other less acute condition and have limited resources in GP ambulance to do complete more detailed diagnostic tests like stress test, laboratory findings, angiography or other procedures that are less often found in GP office. Initial recognition of this symptom but also the future monitoring and treatment of these patients is important for the preventing progression of evolution of the coronary artery disease and progression of stable angina pectoris into unstable angina of myocardial infarction (Adam et al. 2007). In this essay we will conduct a critical review of several studies in order to assess factors that influence the recognition and progression of stabile angina pectoris into a more serious condition. Review of studies in relevance to stabile angina pectoris in primary care As we mentioned above angina pectoris is a symptom defined by the patient in his own words. This condition can often cause changes like ST depression on EKG strip but very often angina pectoris can occur without any changes on the ECG strip (Hausmann et al. 1991). Because more accurate methods for confirmation of angina pectoris are often unavailable in pre-hospital or pre-clinical settings, anamnesis has important function as a factor for initial recognition of this disease. But as we mentioned above angina pectoris is a subjective symptom and description of the patients often vary significantly. This condition was researched by Melvyn et al. 2010 who tried to recognize the variations of presentation of these symptoms. For this task they recruited patients from two general practice institutions and only included patients that had diagnosis for angina pectoris or other ischemic cardiovascular (CV) condition or patients that were taking some form of nitrates. All of the participants were subjected to interview conducted by medical professionals and all of the participants were asked the same questions: did they have any chest, jaw or neck discomfort in the last year and how would they describe this discomfort. A total of 64 patients were interviewed. There are a set of widely accepted individual interpretations of angina pectoris that are called the angina “canon”. These symptoms are (Somerville et al. 2008): - assotiation of the symtoms with physical exercise. - positive reaction after administration of medication, - general duration of symptoms during a single attack. There are studies that show that doctors often don’t ask questions outside these “canonic” interpretations of angina symptoms (Somerville et al. 2008). This fact often results in false negative diagnosis of angina pectoris, by some studies in up to 30 percents of the cases (Sekhri et al. 2007). Melvyn et al. 2010 tried to explore different, “non-canonical” ways patients describe their angina symptoms as breathlessness and attribution of the symptoms to other conditions. For example some patients didn’t mention any chest pain or discomfort but only feeling of breathlessness. Other patients attributed the symptoms to other conditions like “feeling of indigestion” nevertheless patients who were diagnosed with cardiovascular disease. One of the patients attributed the symptoms to ASTHMA or emphysema and the feeling of relief after administration of inhaler (salbutamol). They evaluated also a group of “ambiguous symptoms” that were very random and incoherent individual interpretations by the participant and authors categorize them as vague descriptions, difficulty to describe the symptoms, trying to minimize the symptoms etc. These patients described symptoms that are not suggestive of angina pectoris, however they mentioned those symptoms when they were asked about any chest discomfort, and therefore they assumed that are important about that subject. For example some participants commented that sometimes they feel like the air has been pumped out of their lunges, or “like hard on your chest”, or one participant stated that he loses “breath” when he walks fast and has to stop. As we can see patients often describe their symptoms in a very different ways. These differences author very correctly attribute to several factors. For example maybe “canonical” symptoms are too rigid and don’t fit the wide range of presentations of this condition. Authors also suggest that patients may describe symptoms of some co-morbidities what may be very confusing and misleading to the doctor. Male participants, especially those with previous MI, may try to minimize the symptoms (White and Johnson 2000). Melvyn et al. 2010 in the above mentioned study have shown to us that even though angina pectoris is mainly first recognized in pre-hospital settings and based on the anamnesis of the patient, it is often unrecognized. They suggest that there is a need to spread the “canonic” view of typical presentation of angina pectoris and medical personal must be educated to ask a set of different questions in order to avoid false negative diagnosis of angina pectoris. Above we analyzed a study where the patients were already diagnosed with cardiovascular disease, so the authors knew the diagnosis. This allowed us to monitor the differences in verbal presentation of the symptoms. However we mentioned that those differences between patients can be attributed to arrange of factors, like presence of comorbidities, cultural characteristics, gender or other factors. This may lead to the question what are the most common causes of chest pain in prehospital settings and are there any differences in the presentation of symptoms, differential diagnosis between male and female patents? Stefan et al. 2009 conducted a cross-sectional diagnostic study in primary care patients, involving 74 GP doctors and their patients. Recruited GP doctors had to examine, diagnose and fill standardized questioner regarding chest pain in every patient above 34 years old with chest pain. Importantly every patient already diagnosed with cardiovascular condition or chest pain lasting more that 1 month was excluded from the study. This means that only patients with new onset of chest pain ware included in the study. After this process, study-assistants again contacted every patient after six weeks and six months asking questions about the course of the chest pain, treatments that ware completed in the meantime, medications they were taking, information’s about hospitalization and other medical interventions. After this process a reference panel consisting of one cardiologist and 2 GP doctors reviewed the initial diagnosis and follow up data for every patient and decided about the most common cause of initial chest pain. As we can see this study was trying to explore the accuracy of the initial diagnosis of chest pain, different presentations of chest pain and eventual differences between different groups of patients. A total of 1249 valid participants in this study were included. All of the data were afterwards statistically analyzed for any patterns. Results of this study are interesting. We can see that in the case of 88% of the female and 86% of male patients the main reason for doctor’s visit was a chest pain and both men and women react very similarly on the onset of chest pain, they visited doctors office in high numbers, but only around 30% in the first 48 hours. In the results of this study we can also see that relatively small percentage of all initially registered chest pain was later confirmed as cardiovascular in origin (23% in women and 29% in men). Authors report that there were no differences between men and women in present risk factors for cardiovascular disease (CVD) (diabetes, hypertension, hyperlipidemia, overweight etc.) except for smocking (14.1% males compared to 3.4% females). However there are differences in the ethnology of chest pain. Women suffered more from psychogenic causes of chest pain compared to men, and men suffered more from cardiovascular problems, trauma and pneumonia and/or pleurisy compared to women. There were differences in the clinical presentations of chest pain in patients with confirmed cardiovascular disease. Authors found that chest pain was caused by cardiovascular disease in greater numbers in men compared to women, also men reported more burning pain compared to reported dull pain by women. Also in the most of the patients duration of chest pain was between 1 and 30 minutes, but more women than men reported chest pain lasting between 1 and 12 hours. Both men and women localized the pain in the lower two-thirds of the chest but more men reported right localization of the chest pain. So based on this study we can conclude that both men and women react similarly on the onset of chest pain, and in large percentages patients themselves associated this pain with heart problems, however this was true in less than 30% of the cases. In the study conducted by Melvyn et al. 2010 we found that patients can describe angina pectoris symptoms differently and findings of this study shows that relatively small percentage of reported chest pain in primary practice is from cardiovascular disease, which is confirmed by other studies (Sekhri et al. 2007). This only shows that GP doctors have very important role in initial diagnosis of angina pectoris because they must differentiate any other conditions that may cause chest pain, and in the same time recognize the characteristic but also uncharacteristic manifestations of angina pectoris. Importance of this is well reflected on the study conducted by Sekhri et al. 2007 which found that misdiagnosis is made in 30% of the cases in primary practice. In the previous study we investigated factors that influence the recognition of angina pectoris. However recognition is only the first step in management of this disease. Once diagnosed there are many factors that influence the evolution and progression of angina pectoris to more serious conditions like unstable angina or myocardial infarction. Hjemdahl et al. 2006 are authors of long lasting, very well designed double blind, single-centre trial of the evolution of drug treated angina pectoris in a population of 809 patients over a prolonged period of 9 years. All of the patients had clinical history of stabile angina pectoris and if there was a doubt the diagnosis was confirmed by additional tests in order to exclude any differential diagnosis. All of the patients were randomly treated with either metoprolol or verapamil at recommended doses (Rehnqvist et al. 1996). Authors also note that 39% of the patients used aspirin, 6% used ACE inhibitor, 6% used statins etc. Patients were also monitored for other factors and comorbidities like age, sex, smoking, diabetes mellitus, hypertension, previous angiography or bypass. Even more interestingly authors were able to compare the risks and progression of the disease with reference - healthy population because in Sweden there is complete and up to date population registry that enabled this possibility to the authors. All of the data was statistically analyzed and compared to the reference population. All of the patients had similar demographic and other characteristics, except that smaller percentages of females were smokers and had previous MI compared to men. In the results of this study we find that during the 9.1 years follow up 77 patients died from CVD and 66 were men, 72 had non-fatal MI and 60 were men. Actually authors found that men, but not women had higher mortality rates compared to reference population in the follow up period. They actually found that males had 3-4 times higher risk for major CV event compared to women. However they also found that diabetes mellitus in women was a very high risk for CVD death in women, for example only 14 patients died from 234 non diabetic female patients and 4 patients died from the 16 diabetic patients. Authors also found that advanced age, hypertension, diabetes mellitus, hyperlipidemia were all independently or combined an increased risk factor for cardiovascular event. Authors did not find any differences in prognosis of angina pectoris complications between metoprolol and verapamil groups. With this study we can draw several conclusions. Angina pectoris is more prone to complications in men than in women. This is in concordance with the previous study that we analyzed, where we found that chest pain in males is more commonly a result of angina pectoris than in women. Authors however potentiate that diabetes mellitus comorbidity in women was especially high risk factor and they recommend that this population of women should be closely monitored. Authors also conclude that hypertension and diabetes mellitus are independent risk factors for major CV event. One thing that is interesting in this study is that the same 809 patients in this study were subjected to a number of other research studies over the prolonged period of 9 years. So authors in other study on the same cohort group found that ambulatory ECG ischemia has worse prognosis compared to ischemia detected on exercise (Forslund et al. 1999). Measurements of apolipoprotein A1 levels in this same cohort ware more predictive for major CV event than lipids (Held et al. 1997). Increased levels of mediators of inflammation in the blood ware also a risk factor for major CV event (Held et al. 2000). Based on these researches we can conclude that there are many factors that may influence the prognosis of angina pectoris. However we must attend special attention to comorbidities like hypertension, diabetes mellitus (especially in women), increased BMI, previous MI or other previous major CV event. And based on this study we must pay more attention to male patients more than female. Now this last statement has been a subject of some studies that were trying to investigate if there is a difference in the approach and treatment of males and females with angina pectoris (Mike et al. 2007). Those studies found that male patients are subjected to more investigations and more invasive diagnostic and therapeutic studies when compared to females on every level of the health system, from primary practice to the clinic. Why is this the case, is it a flaw of the health system or we can find some other reasons for it? In a study conducted by Mike et al. 2007 conducted a cross-sectional survey in the primary care in the area of Liverpool in United Kingdom. They based their research on the data obtained by the clinical data managers in private practice. Clinical data managers obtained anonymous data from patients managed in primary care since 1992 and had details about the treatments, therapy and other information’s regarding the treatment. From registered population of 63 724 patients, authors detected 1177 patients with definitive diagnosis of angina pectoris. All of the data was statistically analyzed and authors found important differences between male and female patients. Women with angina pectoris were on average 3.6 years older than man, had a higher frequency of annual physician consultation rates and were on average 4.6 years older at the time of diagnosis when compared to men. Men on the other hand had on average 6 months longer duration of angina and had higher prevalence of previous MI (43% vs. 25%). All patients had secondary prevention where prevention with statins was present in 55%, apirin in more than 84%, beta blocker in 35% (mostly in patients with previous MI) however more men received triple secondary prevention with aspirin, statins and beta blocker. Authors in this study found that men received higher levels of care on every level of health management. Men were significantly more likely to have all risk factors recorded. More men were subjected to diagnostic procedures especially exercise ECG testing, coronary angiography and coronary revascularization. Authors found that women more regularly attended a physician’s visit compared to men, regardless of the fact that fewer risk factors were monitored. What does this mean? We can see that men had earlier onset of angina pectoris and higher incidences of previous MI regardless of the fact that they had better health monitoring than women. Does this mean that if women had the same medical attention their risk would be even smaller? This is something that probable needs further research and lot of factors should be taken into account, like more prevalent CVD in men, incidences of CVD in women, especially after menopause and other factors. In the study we analyzed above we found that angina pectoris is a variable symptom and there are difficulties in recognition of this disease. Also there are difficulties in detecting the risk factors for negative progression of this condition, factors like gender, other comorbidities, previous CV events etc. However there is one widely accepted treatment that become the gold standard in management of angina pectoris and other CV conditions and is broadly available in the primary practice, and that is aspirin. There are a lot of studies that confirm the positive effects of aspirin in reducing the incidence for major CV events. Many clinical trials have shown significantly positive effect of low dose aspirin in prevention of major CV events in stabile angina pectoris. The Swedesh angina pectoris aspirin trial (SAPAT) was the first and to this day most important randomized double blind study of the efficacy of low dose aspirin in prevention of the negative evolution of stabile angina pectoris (Juul-Möller et al. 1992). They used cohort group of 2035 patients with confirmed stabile angina which were randomized in two groups, one with 75 mg aspirin and one placebo group, but all of the patients were taking sotalol for control of the symptoms of angina. The median follow up of the patients was 4 years. In the results of this study authors present 34% reduction of major CV events (myocardial infarction or sudden death) in the aspirin plus sotalol group compared to placebo group. This showed that administration of aspirin resulted in significant reduction of any major CV event in the patients that were taking 75 mg aspirin daily. Authors however noted that in 109 patients the treatment with aspirin was withdrawn because of complications like bleeding, hemorrhagic stroke or other complications which is one important complication of aspirin administration. Based on this study we can conclude that Aspirin is one of the key factors for reducing the risk of complications in patients with stabile angina pectoris. And this fact is confirmed in overwhelming number of other studies that all potentiate the beneficial effects of low dose oral aspirin for control of complications and progression of stabile angina pectoris (Jeffrey et al. 2009). Not just that Aspirin reduces the risk for CV complications but withdrawal from oral aspirin is actually recognized as increased risk factors for future CV events (George et al. 2008). Conclusion Based on the studies that we reviewed in this text we can conclude that primary care has very important role in the treatment of stabile angina pectoris. However there are many factors that influence the recognition and evolution of this condition. We also recognized that male gender, presence of comorbidities, previous CV events are also negative factors. We recognized aspirin as significant factor in reducing the complications of stabile angina pectoris. However there are many more factors that have strong influence on the prognosis of stabile angina pectoris. Moderate physical exercise is associated with decreased risk for live threatening complications of stabile angina pectoris (Michael et al. 2009). Statins are recognized as important factor in reducing major CV events and same as moderate physical exercise can be implemented by primary care doctors (Joel et al 2011). On the end we can only conclude that primary care physicians and nurses have very important role in recognition of stabile angina pectoris but they also have important role in the management and evolution of the disease. Research from the above mentioned studies have shown that there is much to be done in this field in order to improve the recognition of stabile angina pectoris but also implement positive factors that will result in better prognosis of patients with stabile angina pectoris. References: Melvyn M Jones, MD, MSc, MRCGP (2010), Patients' descriptions of angina symptoms: a qualitative study of primary care patients, Br J Gen Pract. 2010 October 1; 60(579): 735–741, doi: 10.3399/bjgp10X532378, PMCID: PMC2944932 Adam D Timmis, Gene Feder, and Harry Hemingway (2007), Prognosis of stable angina pectoris: why we need larger population studies with higher endpoint resolution, Heart. 2007 July; 93(7): 786–791, Published online 2006 September 4. doi: 10.1136/hrt.2006.103119, PMCID: PMC1994448 Hausmann D, Nikutta P, Daniel WG, Wenzlaff P, Lichtlen PR (1991), Anginal symptoms without ischemic electrocardiographic changes during ambulatory monitoring in men with coronary artery disease, Am J Cardiol. 1991 Mar 1;67(6):465-9, PMID: 1998277 Somerville C, Featherstone K, Hemingway H, Timmis A, Feder GS (2008), Performing stable angina pectoris: an ethnographic study, Soc Sci Med. 2008 Apr;66(7):1497-508. Epub 2008 Jan 30, PMID: 18237834 Sekhri N, Feder GS, Junghans C, Hemingway H, Timmis AD (2007), How effective are rapid access chest pain clinics? Prognosis of incident angina and non-cardiac chest pain in 8762 consecutive patients, Heart. 2007 Apr;93(4):458-63. Epub 2006 Jun 21, PMID: 16790531 White AK, Johnson M (2000), Men making sense of their chest pain--niggles, doubts and denials, J Clin Nurs. 2000 Jul;9(4):534-41, PMID: 11261133 Stefan Bösner, Jörg Haasenritter, Maren A Hani, Heidi Keller, Andreas C Sönnichsen, Konstantinos Karatolios, Juergen R Schaefer, Erika Baum, and Norbert Donner-Banzhoff (2009), Gender differences in presentation and diagnosis of chest pain in primary care, BMC Fam Pract. 2009; 10: 79, Published online 2009 December 14. doi: 10.1186/1471-2296-10-79, PMCID: PMC2801475 P Hjemdahl, S V Eriksson, C Held, L Forslund, P Näsman, and N Rehnqvist (2006), Favourable long term prognosis in stable angina pectoris: an extended follow up of the angina prognosis study in Stockholm (APSIS), Heart. 2006 February; 92(2): 177–182, Published online 2005 June 10. doi: 10.1136/hrt.2004.057703, PMCID: PMC1860751 Rehnqvist N, Hjemdahl P, Billing E, Björkander I, Eriksson SV, Forslund L, Held C, Näsman P, Wallén NH (1996), Effects of metoprolol vs verapamil in patients with stable angina pectoris. The Angina Prognosis Study in Stockholm, Eur Heart J. 1996 Jan;17(1):76-81, (APSIS), PMID: 8682134 Forslund L, Hjemdahl P, Held C, Eriksson SV, Björkander I, Rehnqvist N (1999), Prognostic implications of ambulatory myocardial ischemia and arrhythmias and relations to ischemia on exercise in chronic stable angina pectoris (the Angina Prognosis Study in Stockholm (APSIS), Am J Cardiol. 1999 Nov 15;84(10):1151-7, PMID: 10569322 Held C, Hjemdahl P, Rehnqvist N, Björkander I, Forslund L, Brodin U, Berglund L, Angelin B (1997), Cardiovascular prognosis in relation to apolipoproteins and other lipid parameters in patients with stable angina pectoris treated with verapamil or metoprolol: results from the Angina Prognosis Study in Stockholm (APSIS), Atherosclerosis. 1997 Nov;135(1):109-18, PMID: 9395279 Held C, Hjemdahl P, Håkan Wallén N, Björkander I, Forslund L, Wiman B, Rehnqvist N (2000), Inflammatory and hemostatic markers in relation to cardiovascular prognosis in patients with stable angina pectoris, Results from the APSIS study. The Angina Prognosis Study in Stockholm, Atherosclerosis. 2000 Jan;148(1):179-88, PMID: 10580184 Mike Crilly, Peter Bundred, Xiyuan Hu, Lisa Leckey, and Fiona Johnstone (2007), Gender differences in the clinical management of patients with angina pectoris: a cross-sectional survey in primary care, BMC Health Serv Res. 2007; 7: 142, Published online 2007 September 4. doi: 10.1186/1472-6963-7-142, PMCID: PMC2034556 Juul-Möller S, Edvardsson N, Jahnmatz B, Rosén A, Sørensen S, Omblus R (1992), Double-blind trial of aspirin in primary prevention of myocardial infarction in patients with stable chronic angina pectoris. The Swedish Angina Pectoris Aspirin Trial (SAPAT) Group, Lancet. 1992 Dec 12;340(8833):1421-5, PMID: 1360557 Jeffrey S Berger, David L Brown, Gregory L Burke, Albert Oberman, John B Kostis, Robert D Langer, Nathan D Wong, and Sylvia Wassertheil-Smoller (2009), Aspirin Use, Dose, and Clinical Outcomes in Postmenopausal Women with Stable Cardiovascular Disease: The Women’s Health Initiative Observational Study, Circ Cardiovasc Qual Outcomes. 2009 March; 2(2): 78–87, Published online 2009 March 5. doi: 10.1161/CIRCOUTCOMES.108.791269, PMCID: PMC2801891 George Krasopoulos, Stephanie J Brister, W Scott Beattie, R Fraser Elliot and Michael R Buchanan (2008), Aspirin “resistance” and risk of cardiovascular morbidity: systematic review and meta-analysis, BMJ. 2008 January 26; 336(7637): 195–198, Published online 2008 January 17. doi: 10.1136/bmj.39430.529549.BE, PMCID: PMC2213873 Michael McGillion, Philippe L L’Allier, Heather Arthur, Judy Watt-Watson, Nelson Svorkdal, Tammy Cosman, Paul Taenzer, Anil Nigam, Louise Malysh (2009), Recommendations for advancing the care of Canadians living with refractory angina pectoris: A Canadian Cardiovascular Society position statement, Can J Cardiol. 2009 July; 25(7): 399–401, PMCID: PMC2723022 Joel A. Lardizabal, Prakash C. Deedwania (2011), The Anti-Ischemic and Anti-Anginal Properties of Statins, Curr Atheroscler Rep. 2011 February; 13(1): 43–50. Published online 2010 November 24, doi:10.1007/s11883-010-0147-y, PMCID: PMC3018271 Read More