Coronary Heart Disease
Coronary heart disease (CHD), sometimes described as coronary artery disease (CAD) or ischemic heart disease (IHD), is a condition in which the vascular supply to the heart is impeded by atheroma, thrombosis or spasm of coronary arteries. This may impair the supply of oxygenated blood to cardiac tissue sufficiently to cause myocardial ischemia which, if severe or prolonged, may cause the death of cardiac muscle cells. Similarities in the development of atheromatous plaques in other vasculature, in particular the carotid arteries, with the resultant cerebral ischemia has resulted in the term cardiovascular disease (CVD) being adopted to incorporate CHD, cerebrovascular disease and peripheral vascular disease.
Myocardial ischemia occurs when the oxygen demand exceeds myocardial oxygen supply. The resultant ischemic myocardium releases adenosine, the main mediator of chest pain, by stimulating the A1 receptors located on the cardiac nerve endings. Myocardial ischemia may be ‘silent’ if the duration is of insufficient length, the afferent cardiac nerves are damaged (as with diabetics) or there is inhibition of the pain at the spinal or supraspinal level. Factors increasing myocardial oxygen demand frequent precipitate ischemic episodes and are commonly associated with increased work rate (heart rate) and increased workload (force of contractility).
Less commonly, myocardial ischemia can also arise if oxygen demand is abnormally increased, as may occur in patients with thyrotoxicosis or severe ventricular hypertrophy due to hypertension. Myocardial oxygen supply is dependent on the luminal cross-sectional area of the coronary artery and coronary arteriolar tone. Atheromatous plaques decrease the lumen diameter and, when extensive, reduce the ability of the coronary artery to dilate in response to increased myocardial oxygen demand.
Ischemia may also occur when the oxygen-carrying capacity of blood is impaired, as in iron deficiency anaemia, or when the circulatory volume is depleted. CHD kills over 6.5 million people worldwide each year.
Acute Coronary Syndrome
The group of conditions referred to as ACS often present with similar symptoms of chest pain, which is not, or only partially, relieved by GTN. These conditions include acute myocardial infarction (AMI), UA and non-ST-elevation myocardial infarction (NSTEMI). AMI with persistent ST segment elevation on the ECG usually develops Q
waves, indicating transmural infarction. All patients with ACS should be admitted to hospital for evaluation, risk stratification and treatment.
ACS arises from the rupture of an unstable atheromatous plaque. This exposes the cholesterol-rich plaque in the intima to the blood, initiating platelet activation and eventual thrombus formation. The volume of the eventual thrombus and the time the vessel is occluded determine the degree of myocardial necrosis that occurs. The major difference in approach to these patients arises from whether the
coronary artery involved is felt to be occluded or open. Patients with an occluded coronary artery suffer myocardial damage, the extent of which is determined by the duration and site of the occlusion.
The primary strategy for these patients is the restoration of coronary flow with either a fibrinolytic agent or primary angioplasty. If the coronary artery is patent, however, then fibrinolysis is unnecessary and probably harmful, although angioplasty may still be appropriate. When the vessel is open, for both groups, patient management focuses on the unstable coronary plaque and is, therefore, fundamentally similar.
About 3.5% of UK adults have symptomatic CHD. One-third of men aged 50–59 years of age have evidence of CHD, and this proportion increases with age. In the UK, there are about 1.3 million people who have survived a myocardial infarction and about 2 million who have, or have had, angina and this equates to about 5% of men and 3% of women. Approximately 260,000 people suffer a myocardial infarction in any year, of whom 40–50% die. Mortality increases with age and is probably not due to a particular age-related factor but to the cumulative effect of risk factors that lead to atheroma and thrombosis and hence to CAD.
In the USA, age-related death rates for CHD have fallen by 25% over a decade, but the total number of CHD deaths has fallen by only 10% because the population is ageing. Similarly, in the UK the death rates are falling but the numbers living with CHD are increasing. Women appear less susceptible to CHD than men, although they seem to lose this protection after menopause, presumably because of hormonal changes. Race has not proved to be a clear risk factor since the prevalence of CHD seems to depend much more strongly on location and lifestyle than on ethnic origin or place of birth.
Sign and Symptoms
Ischemic heart condition reduces the flow of blood to the coronary arteries, which carry oxygen to the guts. This reduction in blood flow may end in a variety of symptoms, which may vary in intensity among individuals. Common symptoms of ischemic heart disease You may experience ischemic heart condition symptoms daily or just occasionally.
Common symptoms include:
- Chest pain,
- Chest pressure
- Shortness of breath
These are relieved by rest or medicine
They may feel as if pain starting within the chest spreads to the arms, back, or other areas may feel like gas or indigestion (more common in women). If it occurs repeatedly; episodes tend to be alike and occurs when the heart must work harder, usually during workouts last a short time (five minutes or less).
Traditionally, the main potentially modifiable risk factors for CHD have been considered to be hypertension, cigarette smoking, raised serum cholesterol and diabetes. More recently psychological stress and abdominal obesity have gained increased prominence. Patients with a combination of all these risk factors are at risk of suffering a myocardial infarction some 500 times greater than individuals without any of the risk factors. Stopping smoking, moderating alcohol intake, regular exercise and consumption of fresh fruit and vegetables were associated independently and additionally with a reduction in the risk of having a myocardial infarction.
Diabetes mellitus is a positive risk factor for CHD in developed countries with high levels of CHD, but it is not a risk factor in countries with little CHD. Insulin resistance, as defined by high fasting insulin concentrations, is an independent risk factor for CHD in men. In the UK, the mortality rates from CHD are up to five times higher for people with diabetes, while the risk of a stroke is up to three times higher.
While unusual physical exertion is associated with an increased risk of infarction, an active lifestyle that includes regular, moderate exercise is beneficial, although the optimum level has not been determined and its beneficial effect appears to be readily overwhelmed by the presence of other risk factors.
A family history of CHD is a positive risk factor, independent of diet and other risk factors. Hostility, anxiety or depression are associated with increased CHD and death, especially after myocardial infarction when mortality is doubled by anxiety and quadrupled by depression.
Treatment During the Acute Coronary Phase
Once the patient has been diagnosed with acute coronary syndrome (unstable angina or acute myocardial infarction), then they should remain in hospital and rest. If the infarction is due to the total blockage of a coronary artery, then treatment aims to unblock the artery as quickly as possible since every minute counts.
Medicines Used During the Acute Phase are:
Acetylsalicylic acid (aspirin): stops the platelets from aggregating and sticking together inside the artery and therefore reduces the chance of thrombus formation (stationary blood clots). It is the first drug that should be administered at the very onset of chest pain, even while at home.
Other Platelet Aggregation Inhibitors
These reinforce the action of acetylsalicylic acid as they also prevent platelet aggregation. The most common one is clopidogrel, but prasugrel and ticagrelor are also used in particularly severe cases.
By means of a different mechanism; these also aim to dissolve any thrombi (clots) inside the artery. Different types of heparin are used and may be administered by either intravenous or subcutaneous injections.
They work by slowing down the patient’s heart rate, so it is in a more restful state and demands less oxygen. They also reduce the risk of arrhythmias.
Pain Relieving Medicines:
In several cases, patients may require morphine if the pain is very intense.
This can be administered as a tablet, sprayed underneath the tongue or by intravenous injections. It is used to dilate the heart’s arteries allowing more blood to flow through them.
Thrombolytic or Fibrinolytic Agents
In cases where a thrombus is completely blocking an artery, these drugs can be administered in order to break the clot down and thin the blood.
Drug Therapy of Coronary Heart Disease
Patients with Ischemic heart condition must take a mixture of medicine to scale back the heart’s oxygen consumption, dilate the coronary arteries and stop the formation of a replacement blockage. Nitro-glycerine and its derivatives (nitrates, either as tablets or transdermal patches): these drugs are known as vasodilators. They relax the arteries and veins, including the coronary vessels, thereby increasing blood flow within the affected area and eliminating pain from angina.
Beta-blockers (bisoprolol, carvedilol, nebivolol, metoprolol, atenolol, etc.):
Decrease vital signs and pulse, hence the guts require less oxygen to function correctly. They can also reduce the risk of arrhythmias. Studies have shown that beta-blockers can increase the life expectancy
of patients who have had an infarction.
Platelet Aggregation Inhibitors
Patients who have suffered any event brought on by atherosclerosis must take platelet aggregation inhibitors
permanently unless they are contraindicated. These drugs stop platelets from clumping together which has the effect of thinning the blood and reduces the risk of thrombus formation inside a coronary artery.
These drugs reduce blood cholesterol levels. They also help stabilise and prevent the rupture of atheromatous plaques, reduce blood vessel inflammation and decrease the likelihood of an infarction.
Other anti-anginal agents are calcium channel blockers, relax the muscles of the coronary arteries and mitigate the consequences of obstructions and spasms.
Treatment is tailored to each patient; the drugs and doses may vary greatly from one person to the next. It is important that you know what treatment you are prescribed so you can inform the doctor if you are
treated for Ischemic Heart Disease.
- Haemorrhagic stroke of unknown origin at any time
- Ischemic stroke in the preceding 6 months
- CNS damage or neoplasms
- Recent major trauma/surgery/head injury (within preceding 3
- Gastrointestinal bleed within the last month
- Known bleeding disorder
- Non-compressible punctures
- Aortic dissection
- Transient ischemic attack in the preceding 6 months
- Oral anticoagulant therapy
- Pregnancy or within 1 week postpartum
- Advanced liver disease
- Active peptic ulcer
- Infective endocarditis
- Traumatic resuscitation
- Refractory hypertension (systolic blood pressure >180mmHg)
Management of Complications
Heart failure. Heart failure during the acute phase of STEMI is associated with a poor short- and long-term prognosis. It should be managed with oxygen, intravenous furosemide and nitrates. More severe failure or cardiogenic shock (tissue hypoperfusion resulting from cardiac failure with symptoms of hypotension, peripheral vasoconstriction and diminished pulses, decreased urine output and decreased mental status) should be treated with inotropes and/or inter-aortic balloon pumps to maintain the systolic blood pressure above 90mmHg. Invasive monitoring may be required.
Life-threatening arrhythmias such as ventricular tachycardia, sustained VF or atrio-ventricular block occurs in about one-fifth of patients presenting with a STEMI, although this is decreasing due to early reperfusion therapy. β-Blockers have been the subject of many studies because of their anti-arrhythmic potential and because they
permit increased subendocardial perfusion. In studies undertaken prior to the widespread use of fibrinolytics, the early administration of an intravenous β-blocker was shown to limit infarct size and reduce mortality from early cardiac events.
β-blocker is contraindicated because of respiratory or vascular disorders, verapamil may be used since it has been shown to reduce late mortality and reinfarction in patients without heart failure, although it shows no benefit when given immediately after an infarct.
Patients with a myocardial infarction are often found to have high serum and urinary glucose levels, usually described as a stress response. The CREATE-ECLA trial studied more than 20,000 patients and showed a neutral effect of insulin on mortality, cardiac arrest and cardiogenic shock. Current guidelines do not support the routine use of insulin in STEMI in patients not previously known to be diabetic.
Patients with CHD range from those who have investigational evidence of CHD but no symptoms to those who have major pain and exercise limitation. All need encouragement in adhering to preventive measures including diet, exercise and smoking cessation. Patients need to be able to discuss concerns about their health.
Exercise must be tailored according to the patient’s threshold for angina. In general, although some patients are too cavalier, most are likely to err on the cautious side and may need to be encouraged to do more. Many centers now run cardiac rehabilitation classes to encourage patients to exercise and adopt a suitable lifestyle. There are simple treatments and important lifestyle changes that can reduce cardiovascular risk and slow or even reverse progression of established coronary disease.
The most important of these to address is smoking cessation. The risk of CHD is two to four times higher in heavy smokers (those who smoke at least 20 cigarettes/day) than in those who do not smoke. Other reports estimate the age adjusted risk for smokers of more than 25 cigarettes/day is 5-21 times that of non-smokers. Smokers should be encouraged to quit. Within months of stopping smoking, CHD risk begins to decline. Within 5 years of smoking cessation the risk decreases to approximately the level found in people who have never smoked, regardless of the amount smoked, duration of the habit and the age at cessation.
The use of nicotine replacement therapy almost doubles a smokers’ chance of successfully stopping smoking (18% vs. 11%). All patients who smoke should be offered advice on cessation and encouraged to attend specialist smokers & 39% clinics to further improve their chance of quitting
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