Heart attack can be prevented
By Professor Mohammad Ishaq
Matters of the heart should not be taken lightly, especially when signs tell that an attack is on its way
ISCHAEMIC heart disease (IHD) is rated as the No1 killer of adult population worldwide. Epidemiological studies have found South East Asia (Pakistan included) as the high risk region for IHD. Acute myocardial infarction (AMI) popularly known as heart attack is the main mode of presentation of Ischaemic heart disease (IHD) in the hospital as an emergency event. Acute myocardial infarction (AMI) carries very high mortality and morbidity. Fortunately over the past three decades, tremendous advancement in the diagnosis and management of IHD has taken place.
Each day every hospital casualty department certifies a number of patients who are dead on arrival (DOA). This is what we call the syndrome of sudden cardiac death (SCD). Unfortunately none of these patients undergo autopsy (post mortem examination) and therefore the precise cause cannot be established in our community.
CAUSES OF SCD
Acute myocardial infarction (AMI)
Cardiac arrhythmias
Cardiogenic shock
Acute heart failure (HF)
Heart rapture
Severe valvular stenosis
Idiopathic heart muscle disease (Cardiomyopathies)
WHO ARE PREDISPOSED TO SCD:
Following groups of individuals have high susceptibility towards sudden cardiac death.
Individuals with known IHD (previous heart attack, angina, etc).
Individuals with known arrhythmias (Supraventicular/ventricular tachy arrhythmias).
Individuals with heart failure (significant left ventricular dysfunction).
Individuals with known family history of heart disease and sudden death in the family.
Individuals who carry risk factors like high blood pressure, diabetes mellitus, hypercholestrolaemia, smoking, obesity and sedentary living.
Someone dying all of sudden is a very serious and dramatic event, one which has catastrophic consequences for the individual, family and the community at large.
The question arises can we do something to prevent such a catastrophe. The answer is yes we can do so ‘something’.
* INDIVIDUALS with known IHD should stick to the physicians prescription, advice regarding life style modification and further tests. They should comply with the specialist’s recommendation regarding angioplasty or coronary artery bypass surgery. Drugs like aspirin should be taken for life. Blood pressure, cholesterol and sugar lowering drugs should be taken on long term basis and only stopped on the advice of the physician. Those who have undergone interventional (angioplasty) or surgical (coronary artery bypass surgery) procedures should follow the postoperative do’s and don’ts, religiously. They should attend for follow up visits on the scheduled dates and should not carry the impression that all is over. It should be borne in mind that IHD is at best only controlled but not cured.
* INDIVIDUALS with known arrhythmias whether primary or secondary should receive long-term antiarrhythmic medications. These medications need to be properly monitored and their dosage adjusted accordingly. There are four classes of antiarrhytmic agents and almost all sorts of arrhythmias can be controlled with appropriate pharmacotherapy. In addition to anti-arrhythmic medications, a number of interventional and surgical procedures can be adopted which cure or suppress the tendency towards arrhythmias.
* INDIVIDUALS with significant LV dysfunction or overt heart failure (HF) are at high risk for SCD. The main cause for sudden death in heart failure patients is intractable arrhythmias, thrombotic episodes and cardiac rupture. These patients need to be kept on long term anti-arrhythmic, anti-coagulant and anti-failure treatment. Some of them may benefit from surgical treatment and assist devices.
The heart failure population is on the rise due to improved survival after myocardial infarction which is the result of advancement in pharmacological and interventional treatments. Despite excellent pharmacological agents, management of heart failure remains a major challenge and still carries very high mortality and morbidity.
* INDIVIDUALS with no clinically manifested IHD, but still carrying risk factors like hypertension, diabetes mellitus, hyperlipidaemia, obesity, smoking and sedentary living. Such individuals are potential candidates for IHD at some stage in their life. They are also predisposed to sudden cardiac death. Such individuals should modify their risk factors through life style modification and where necessary with medicines. They should also get themselves properly checked and investigated. Those who are over forty with any of the above major risk factors should preferably undergo an elective exercise tolerance test (ETT) to rule out the possibility of latent heart disease.
Persons suffering from diabetes mellitus need special attention. Diabetic sufferers of IHD have special features. They often lack the typical chest pain and can have ischaemic events including myocardial infarction in the absence of pain (silent angina or heart attack).
ETT is an excellent screening test but is by no means 100 per cent specific or sensitive. Therefore it has be read with caution and whenever in doubt patients must undergo advance test like thallium scan and coronary angiography.
To summarize, sudden death needs to be recognized as a disease entity rather than just an accident or a matter of destiny. Majority of SCD occur in people with IHD weather manifest or latent. Most of the patients with manifest IHD are under some form of treatment and therefore enjoy some degree of protection. Whereas the individuals with latent (non manifest) or diagnostically missed IHD are specially prone to SCD as they are neither taking any medicines nor practising any preventive measures.
It is the duty of the medical profession to identify such individuals prior to the catastrophe. This needs great deal of public awareness and professional expertise. Family physicians are the best persons who can identify people at high risk and refer them to the specialist after preliminary tests.
A number of heart attack patients can be saved from SCD if they receive prompt medical attention. Community (family) physicians need to be trained in very early management of heart attacks including defibrillation (D.C. cardioversion). The way the IHD is spreading in our community there is a dire need for more and more local emergency cardiac centres. A number of patients are dying while on their way to major hospitals due to transit time and logistical reasons.
Tertiary care centres cannot be established in every corner of the city but centres with emergency cardiac facilities capable of dealing with early phase of acute chest pain can be provided in various zones of the metropolitan cities.
The solution of IHD problem lies in its prevention. Preventive measures must be reinforced all the time and all efforts made to identify high risk persons. Once identified the management of high-risk individuals is the responsibility of family, family physicians and the specialist involved. Every effort must be made to preempt the catastrophic events including SCD. Death is a reality and we all have to embrace it but some untimely deaths can be averted by adhering to above measures. A single individual saved through preventive means is a 100 per cent success for that individual.
From platelets to heart attacks
By Dr Sheikh Arshad Saeed
CARDIOVASCULAR disease, heart disease and stroke are overwhelmingly the leading cause of death for men over the age of 30 and women over age 40. More importantly, one-third of the heart attack victims do not survive the first attack.
Heart is a fist-sized organ that pumps over 2000 gallons of blood through the circulatory system each day by contracting and relaxing more than 100,000 times. The ability of heart to function as an efficient pump is dependent on an adequate blood supply to its muscular walls (the myocardium). When myocardial blood supply is reduced (ischemia), the contractile function of the heart is impaired. Prolonged ischernia may result in cellular damage which can lead to myocardial cell (infarction) leading to contractile failure (heart failure).
The primary cause of heart trouble is atherosclerosis, or clogging of the arteries of the heart. This process starts in early childhood as a result of mechanical injury, or chemical damage (e.g. lipids) to coronary vessels endothelium (the thin lining of cells inside all blood vessels). A plaque made up of cholesterol and scar tissue clogs the arterial walls.
Initially only a fatty streak may be formed, which after many years develops into atherosclerotic plaques. The real danger comes when smaller plaques gets ruptured. That leads to the activation of platelets (a blood component) and their aggregation causing blockage of coronary arteries and myocardial ischernia (myocardial ischemia).
Platelets are basically tiny, quiescent blood particles lacking a nucleus. Abundant in circulation (about 200-400 billion per litre of blood) and having a life span of seven days, their main function is to control bleeding. Bone marrow cells called megakaryocytes are taken as platelets precursors. In healthy individuals, a fine balance is maintained in regulating platelet function, preventing excessive blood clotting (thrombosis) on one hand and excessive bleeding (haemorrhage) on the other. This process is altered in people suffering from heart attacks and sudden platelet aggregation is now taken as primary mechanism in acute incidents of ischernic heart disease.
In support of this, the frequency of myocardial infarction and sudden death in man is known to increase during early hours of the morning and this correlates with increased ability of platelets to aggregate. Also, the incidence of atherosclerosis increases with age, and this is associated with the observation that platelets from elderly people are more sensitive to aggregatory stimuli.
These findings have aroused great interest in evolutionary biologist who are now looking at this phenomenon from an evolutionary perspective. The closed circulatory systems of humans and mammals with blood clotting mechanisms have taken 30 million years to develop.
For researchers, the focus is no longer on how to shrink or stop these plaques from forming, which is nearly impossible, but to make these plaques rupture-resistant. Anti-platelet therapy now provides us with a solution to this problem. This knowledge has really changed the thinking and direction of our care to prevent heart disease.
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