Introduction
Coronary heart disease (CHD) is a condition where the blood supply to the heart is blocked or interrupted due to fatty substances building up in the blood vessels. Which are responsible for blood delivery to the heart, they are called coronary arteries. This is also why CHD is sometimes called coronary artery disease. The build-up of fatty plaques can block blood flow to the heart, and therefore less oxygen. This means that the heart cannot contract; the reduction of oxygen supply will lead to some of the symptoms of CHD.
The most common symptom of CHD is angina, a pain usually felt in the chest. It is due to reduced blood flow to the heart. Though angina is not life-threatening, it can signify that the person is at risk of experiencing a heart attack or stroke, which are both deadly.
The risk factors of CHD include:
- Smoking
- high blood pressure (hypertension)
- high cholesterol
- high levels of lipoprotein (a)
- Sedentary lifestyle
- Diabetes
- Obesity or being overweight
- Family history of CHD
CHD is responsible for the deaths of 9 million people every year. It is estimated that around 200 million people are living with CHD around the world, and around 110 million of them are men, and 80 million are women.
It is important that the condition is taken care of to prevent heart attacks, anginas and heart failures, which can be sudden or gradual. Both heart attacks and heart failures can be fatal. CHD can be managed by changing the diet and lifestyle, taking medications, angioplasty (placing an inflatable balloon or expandable metal coil into the arteries) and heart surgeries.
CHD medications generally aim to reduce blood pressure, widen the arteries or prevent blood clotting. These medications should not be stopped without doctors’ advice, as it can worsen the symptoms.
Types of medications used in CHD management
Antiplatelet agents
Overall, antiplatelet agents work by preventing platelet cells from functioning, and as a result, the blood is less likely to form a clot.
Platelet cells are an important group of blood cells that circulate in the body to help with blood clotting. However, they are less helpful in CHD. When the fatty plaque that builds up in major arteries ruptures the body will naturally want to clot at the site of the rupture. The clot will likely block blood delivery in the arteries to the heart, and without oxygen being delivered to cardiac muscle, this will lead to heart failure.
Antiplatelet cells can disturb the stomach lining; therefore, patients taking the medication may develop stomach aches or even stomach ulcers. Proton pump inhibitors may need to be taken to protect the gastric lining.
Aspirin
Aspirin is the most common antiplatelet drug given to patients with CHD. It is usually prescribed after a heart attack for life. When, why, and how prescribed. A bit more info here would be helpful.
For more obvious side effects, patients may experience nose bleeds and get bruised more easily, since it is harder for the blood to clot.
P2Y12 inhibitors (e.g. Clopidogrel)
P2Y12 inhibitors are usually prescribed with aspirin to patients with stent placement (a stent is a piece of expandable mesh coil that opens up a narrow section in artery to allow more blood flow, and plaques can form around the metal stent) in arteries or patients that require stronger blood clotting.1 They target receptors on platelet cells and prevent the receptors from activation, thus stopping platelet cells from dividing.
Similar to the negative effect of aspirin on gastric lining, however, unlike aspirin, P2Y12 inhibitors like Clopidogrel cannot be taken alongside proton pump inhibitors which suppresses stomach acid which was said to reduce the effectiveness of the inhibitor.
Beta-blockers
Beta-blockers reduce the risk of heart attacks essentially by reducing heart rate and oxygen demand. Beta-blockers work by blocking beta receptors, which exist in different forms: beta 1,2, 3. The main blocker that is prescribed to CHD patients targets the beta-1 receptor (B1) which is located in the heart and mediates cardiac activity. Hormones bind to the B1 receptor to increase the heart rate, as well as the force of contraction and oxygen demand, which will worsen the imbalance in oxygen supply to heart muscle for CHD patients. So when beta-blockers are taken, all the described effects are inhibited, thus the risk of angina is decreased.
Because beta-1 receptors are located in other organs other than the heart for example kidney and the fat cells, it may cause adverse effects in these organs as well. Some of the most reported side effects include:
- Fatigue
- Dizziness
- Nausea
- Constipation
ACE inhibitors and ARBs
ACE Inhibitors (e.g., enalapril, lisinopril)
ACE Inhibitors stands for angiotensin-converting enzyme inhibitors (ACEI) and is another CHD medication that treats hypertension. The enzyme functions as suggested by the name converts a hormone called angiotensin into its active form, which will constrict the blood vessels, leading to hypertension2. When the enzyme is inhibited by its inhibitor, the blood vessels will relax and dilate. The blood pressure and flow to the heart muscle are therefore improved. The cardiac output is improved, which means the heart works more efficiently without increasing the heart rate; the drug takes off the pressure on the heart when it contracts.
Since a quarter of blood pumped out from the heart goes to the kidney, improving the efficiency of the heart will improve kidney function as well.
Around 1 to 10% reported having a dry cough after taking the medication; unfortunately, there is no treatment for the cough.3 Salt is known to increase blood pressure, and it also specifically interferes with the effect of ACE inhibitors, so patients should be mindful of salt intake while taking ACE inhibitors.
Angiotensin II receptor blockers (ARBs) (e.g., losartan, valsartan)
ARBs achieve the same overall effect as ACEI. ACEI reduces the amount of activated angiotensin, angiotensin II, from being produced. ARBs, conversely, block the receptors of angiotensin II, so they are not detected. ARBs are usually prescribed when the dry cough caused by ACEI does not go away.
Statins
Cholesterol is an important cellular component that plays a key role in maintaining the integrity of cells, and they are precursors of vitamin D and steroid hormone synthesis. There are two types of cholesterol: the good ones (high-density lipoprotein) and the bad ones (low-density lipoprotein). When the bad cholesterol level is too high, it can cause more fatty plaque to form in the arteries, blocking the blood flow.
Statins are inhibitors that lower total cholesterol levels, decrease the “bad” cholesterol and increase “good” cholesterol. Statins do this by inhibiting an enzyme that is a key in cholesterol synthesis: HMG-CoA reductase.4
Statins are classified in terms of intensity:
- Low-intensity statins reduce LDL-C by less than 30%
- Moderate-intensity statins: reduce LDL-C by 30 to 50%
- High-intensity statins: High-intensity statins reduce LDL-C by greater than 50%.
There are also different types of statins, and they have different concentrations within each intensity:
- Atorvastatin (Lipitor)
- Fluvastatin (Lescol)
- Pravastatin (Lipostat)
- Rosuvastatin (Crestor)
- Simvastatin (Zocor)
It is not always the default option to start statin therapy at the highest intensity as it is associated with stronger adverse effects; patients need to be moderated regularly to see if they are sensitive to a particular statin, and blood tests should be taken to monitor the level of cholesterol.
Nitrate
Nitrates can dilate the blood vessels, reducing blood pressure. When nitrate is in the system, they are converted to nitric oxide by enzymes. Nitric oxide is usually provided by the inner lining of blood vessels, however, in patients who have fatty plaque build up on their arterial walls, this process is hindered. The release of nitric oxide ultimately leads to the relaxation of smooth muscle in the blood vessels.5
Personalised medication regimens
When designing drug treatment, doctors have taken into account the individual’s need and their health situation. If the patient also has other comorbidities. For example, for kidney disease, ACEI OR ARB might be chosen as both medications have protective functions on the kidney. individuals with high blood pressure are usually given ACE inhibitors, ARBs, or beta-blockers. Diabetics with CHD benefit by taking Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitors, which are usually for diabetics but have an emerging cardiovascular benefit.
Genetics is closely linked with CHD. Genetic tests are conducted for risk calculation, prediction of treatment efficacy, and detection of subjects prone to drug side effects.6 Certain genes can give manifestations to significant CHD risk factors, like high concentrations of LDL, diastolic dysfunction and right ventricular failure.6
Conclusion
The pharmacological management of coronary heart disease (CHD) is a complex strategy that targets many components of the condition, including blood pressure reduction, blood clot prevention, and cholesterol control. Drugs, including beta-blockers, ACE inhibitors, statins, and antiplatelet medicines, are essential for enhancing heart health, easing symptoms, and averting major problems like heart attacks or strokes.
In order to maximise results, treatment strategies must be customised to each patient's unique risk factors and comorbidities. Individualised medicines, based on genetic testing and cutting-edge technologies, hold the promise to substantially improve the management of this common ailment as our understanding of CHD and pharmacology increases.
References
- Angiotensin-Converting Enzyme - an Overview | ScienceDirect Topics. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/angiotensin-converting-enzyme#:~:text=Angiotensin%2Dconverting%20enzyme%20(ACE)%20is%20a%20transmembrane%20zinc%20metallopeptidase,vasoconstrictor%20angiotensin%20II%20%5B55%5D. Accessed 7 Sept. 2024.
- Bansal, Agam B., and Manouchkathe Cassagnol. ‘HMG-CoA Reductase Inhibitors’. StatPearls, StatPearls Publishing, 2024. PubMed, http://www.ncbi.nlm.nih.gov/books/NBK542212/.
- Herman, Linda L., et al. ‘Angiotensin-Converting Enzyme Inhibitors (ACEI)’. StatPearls, StatPearls Publishing, 2024. PubMed, http://www.ncbi.nlm.nih.gov/books/NBK431051/.
- Lee, Peter M., and Valerie Gerriets. ‘Nitrates’. StatPearls, StatPearls Publishing, 2024. PubMed, http://www.ncbi.nlm.nih.gov/books/NBK545149/.
- Pradhan, Akshyaya, et al. ‘Ideal P2Y12 Inhibitor in Acute Coronary Syndrome: A Review and Current Status’. International Journal of Environmental Research and Public Health, vol. 19, no. 15, July 2022, p. 8977. PubMed Central, https://doi.org/10.3390/ijerph19158977.
- Vrablik, Michal, et al. ‘Genetics of Cardiovascular Disease: How Far Are We from Personalized CVD Risk Prediction and Management?’ International Journal of Molecular Sciences, vol. 22, no. 8, Apr. 2021, p. 4182. PubMed Central, https://doi.org/10.3390/ijms22084182.

