The most important determinant of cardiovascular health is person’s age. The average lifespan of humans is increasing, and with it, the percentage of people entering the 65 and older age group is growing rapidly. Elderly healthy individuals have a reduced cardiac output, reduced exercise tolerance and a decreased left ventricle inotropic reserve. This is due to increased vascular after load, arterial ventricular load mismatching, physical deconditioning due to impaired autonomic regulation and “β- adrenergic desensitization”. These changes in cardiovascular physiology must be differentiated from the effects of pathology, such as coronary artery disease (1, 2).

Advanced age is the single strongest non-modifiable risk factor for coronary artery disease (CAD) and independent predictor for poor outcomes following an acute coronary syndrome (ACS). ACS refers to a spectrum of conditions compatible with acute myocardial ischemia and/or infarction due to various degrees of reduction in coronary blood flow due to plaque rupture/erosion and thrombosis formation or supply and demand mismatch (3). Acute myocardial infarction (AMI) occurs when there is prolonged ischemia, caused generally by coronary athero-thrombosis resulting in irreversible damage to the segment of the cardiac muscle supplied by the subtended artery.

The WHO has proposed 3 criteria for making the diagnosis of AMI namely: 1) Typical chest pain, 2) Increased cardiac enzymes, 3) Electrocardiographic changes. The major modifiable classical risk factors for m yocardial infarction include smoking, hypertension, diabetes mellitus and obesity. In all these classical risk factors there is co-existence of autonomic nervous system dysfunction. Typical angina symptoms predictive of AMI are less helpful in diagnosing AMI in the elderly population (3). Autonomic symptoms such as dyspnoea, diaphoresis, nausea and vomiting, pre-syncope or syncope are more common accompaniments to chest discomfort in elderly AMI patients (3). The elderly with AMI have been reported to present with more atypical symptoms (4, 5). AMI is associated with significantly higher mortality in the elderly compared with the young (5). Hence, high index of suspicion for AMI, along with an appreciation of its context, must be maintained in assessing elderly patients to achieve timely diagnosis and appropriate management (3).

The younger age generation is characterized by a marked increase in the intake of energy-dense foods, a decrease in physical activity, and heightened level of psychosocial stress (6). An examination of patients with non ST-segment elevation myocardial infarction revealed that 9% were found to have insignificant coronary artery disease, suggesting a pathophysiological mechanism distinct from progressive plaque rupture that may drive acute coronary syndrome event (7). Hypercoagulable states (high fibrinogen, high D-dimer) also have been associated with premature acute coronary syndrome (8-10).

There is disparity in the literature on the definition of young with respect to premature AMI. The term young age with respect to AMI varies from 40 years to 55 years of age (11-14). Till date not much data available on myocardial infarction patients in Mysuru city. There is a need for research on cardiovascular ageing, which can lead to better understanding of cardiovascular diseases. Hence, we hypothesise that, in old age patients there is risk of autonomic nervous system dysfunction causing a typical clinical presentation of AMI patients. Thus, in this study we have compared the differences in classical risk factors and clinical features between young and older AMI patients.

Objective of the study:

The aim of this study is to compare the classical risk factors and clinical features between young age and old age patients with acute myocardial infarction.

This study is a retrospective comparative study. This study was conducted with prior approval from the Institutional Ethical Committee of JSS Medical College and Hospital. The patients data recorded in the acute coronary syndrome (ACS) register of JSS hospital, Mysuru from December 2015 to December 2016 was analysed.

Inclusion criteria

1. The patient aged more than 35 years, but less 70 years old.
2. Patients with first or consequent acute myocardial infarction. The Myocardial infarction as confirmed by standard definition (symptoms, cardiac enzymes and electrocardiographic changes) (15).

Detection of rise/fall of cardiac biomarker values (such as CPK, CK-MB, troponin I, high sensitive cardiac troponin (hs-Tn)) with at least one value above the 99th percentile upper reference limit (URL) and with atleast one of the following:

1. Symptoms of ischemia
2. New or presumed new significant ST-segment-T wave (ST-T) changes or new left bundle branch clock (LBBB)
3. Development of pathological q-waves
4. Imaging evidence of new loss of viable m yocardium or new regional wall m otion abnormality
5. Identification of an intracoronary thrombus by angiography.

Exclusion criteria:

1. The patients ageless than 35 years and more than 70 years.
2. The patients who do not meet the universal definition of Myocardial infarction.
3. The patients with diseases such as severe valvular diseases, recurrent ventricular arrhythmias, heart failure (NYHA class 4), cancers, severe aortic incompetence, severe atrial fibrillation, end stage renal diseases and end stage liver diseases.

Group: (I) A set of 40 patients with acute myocardial infarction (age <50 years) was taken as young age group.

Group: (II) A set of 40 patients with acute myocardial infarction (age >51 years) was taken as old age group.

Statistical analysis:

Statistical analysis was carried out using SPSS software. The percentage of patients with classical risk factors was calculated. This includes percentage of patients with diabetes mellitus, hypertension, dyslipidaemia, obesity and smoking. The odds ratio was calculated for number of smokers in the two groups. Similarly, the percentage of patients with typical chest pain, increased cardiac enzymes, electrocardiographic changes (15), were calculated in the two groups. The mean values and standard deviation of LDL, HDL, Troponin T, and CK-MB levels were calculated in both the groups. Both groups were compared by unpaired t-test. A p value <0.05 was considered to be statistically significant.

In the young age group patients, single vessel disease was most prevalent, with the lesion most commonly located in the left anterior descending artery. In most studies, smoking was the major risk factor for AMI in young men and women (16-18). In both the groups evaluated, the most common risk factors, identified were dyslipidaemia, and BMI < 25 kg/m².
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In the old age patients the adaptations of cardiovascular system to stress are impaired as a consequence of physiological and metabolic changes in the cardiovascular system itself. This leads to increase in impedance to ventricular ejection due to atherosclerotic changes in the arteries and insufficient vasodilatory capacity of the peripheral blood vessels. Age-related changes occur throughout the arterial wall. The arterial tree is a visco-elastic tube. In younger individuals, the central arteries are more elastic and less stiff than the peripheral arteries. Com pared to vessels from healthy younger individuals, arteries from older individuals are characterized by increased reactive oxygen species (ROS) content, inflammatory changes, decreased NO availability, and endothelial dysfunction. Increased arterial stiffness secondary to atherosclerosis causes decreased elasticity of the aorta and great arteries (19). Ageing is associated with a decline in aortic distensibility and with increased aortic stiffness as measured by pulse wave velocity (PWV). This strongly suggests that arterial stiffness is mainly driven by ageing process (19, 20). These ageing associated cardiovascular-physiologic changes cause left ventricular dysfunction.

There are significant age-related changes in autonom ic nervous system function that are responsible for an impaired ability to adapt to environmental or intrinsic visceral stimuli in the elderly. The influence of physiological ageing also causes attenuated baroreflex and autonomic reflexes due to the decreased responsiveness to â-adrenergic receptor stimulation (1, 21). The chronic diseases such as diabetes mellitus or hypertension are associated with autonom ic nervous system dysfunction. The coexistence of these chronic diseases in old age patients causes the clinical features of m yocardial infarction to be uncharacteristic. In the present study more cases among the old age patients had atypical chest pain with other nonspecific autonomic symptoms like nausea, vomiting, giddiness, syncope and palpitation on admission to hospital as compared to young age patients. This is because the old age patients appear to have reduced pain perception. This phenomenon may result from the increase of pain threshold of permanently ischemic sensory nerves, ischemic dysfunction of the cerebral cortex, and dysfunction of the autonomic nervous system (16). The patients of AMI are treated by either by thrombolysis or coronary angioplasty should undergo cardiac rehabilitation (CR). It is the process of restoring desirable levels of physical, social, and psychological functioning after the AMI. These CR programs provide patient education, identify and monitor risk factors. It also helps in lifestyle modification such as cessation of smoking, and enhances exercise training for patients with AMI. These programs are tested and proven to be beneficial to both young age and old age group of AMI patients (22, 24). The research on cardiovascular ageing can lead to new view and better understanding of cardiovascular diseases (23).

Conclusion:

Smoking and dyslipidaemia are the most important modifiable risk factors and can be the targeted to reduce the rate of myocardial infarction in the young age patients (22). In the old age patients with AMI, the influence of physiological ageing causes autonomic nervous system dysfunction and presents m ore com m only with a typical chest pain, hypertension, diabetes mellitus, and left ventricular diastolic dysfunction (3, 24).