Drugs for Coronary Artery Disease and Angina

Large veins relax, causing vasodilation.

Widening of blood vessels.

Blood flowing back to the heart from the veins.

More venous blood returning to the heart means more blood for the heart to pump.

Increased blood flow leads to a higher heart rate.

The pressure of blood within the blood vessels.

Increased blood flow/blood volume to the heart increase the heart's need for oxygen.

The heart works harder to pump more blood.

Propranolol, a beta-blocker, can be used to prevent angina by reducing heart rate and myocardial contractility, thereby lowering oxygen demand.

Angina can be "typical" (exertional) or "variant" (at rest).

Beta-blockers are good for long-term prevention of typical angina, but less suitable for variant angina due to potential side effects.

Calcium channel blockers relax arteries and reduce the force of myocardial contraction, thus decreasing the heart's workload and oxygen demand thereby improving angina.

Calcium channel blockers are crucial for preventing variant angina, typically preferred over beta-blockers for this condition.

Chest pain caused by reduced blood flow to the heart muscle.

A class of medications that decrease heart rate and blood pressure to lower heart's oxygen requirements.

Medications that reduce the heart's workload by relaxing blood vessels to improve blood flow.

The force of the heart muscle's contraction.

Blood vessels supplying the heart muscle with blood.

Chest pain brought on by exertion (physical activity).

Chest pain occurring at rest.

When the heart has to work harder than normal, potentially causing pain, a symptom of angina.

The amount of oxygen needed by the heart to function.

Prevention of a condition or disease.

Activation of the Renin-Angiotensin-Aldosterone System (RAS) that leads to elevated blood pressure (BP).

Sustained stimulation of beta receptors in the heart due to sympathetic nervous system (SNS) activation.

Protease enzymes linked to programmed cell death (apoptosis) and inflammation.

A hormone that constricts blood vessels and contributes to cardiovascular remodeling.

Changes in the structure of the heart and blood vessels, often a negative adaptation to stress.

The death of heart muscle cells, a key component of heart failure.

The heart's initial attempt to maintain output by increasing muscle mass.

Temporary improvement in cardiac output, during the initial phases of heart failure.

Eventually, the heart's increased effort contributes to more severe heart failure.

Treatment goals seek to manage the symptoms and underlying causes of heart failure.

This type of treatment involves lifestyle changes and procedures that don't involve medication.

These are changes in daily habits that can improve heart health. Examples include increased physical activity, dietary control, and stress management.

This involves making changes to your eating habits to reduce sodium intake and overall calorie consumption.

This involves procedures to improve blood flow to the heart, such as coronary revascularization and cardiac transplantation.

This involves using medication to manage heart failure. Examples include diuretics, vasodilators, and positive inotropic agents.

These medications help the body eliminate excess fluid and salt, reducing blood volume and workload on the heart.

These medications relax blood vessels, reducing blood pressure and improving blood flow.

These medications block the renin-angiotensin system, which helps control blood pressure and reduce strain on the heart.

These medications increase the heart's contractility, improving its pumping ability.

Digoxin can alter intracellular potassium levels by competing with potassium for binding sites on the sodium-potassium ATPase pump. This competition influences the activity of digoxin.

Certain antibiotics, like erythromycin, can interact with digoxin and affect its activity. This is because these antibiotics can inhibit the metabolism of digoxin, leading to increased levels in the body.

Visual disturbances might signal problems with the nervous system. The brain can be affected by changes in blood sugar or medications, potentially leading to hallucinations or illusions. Be aware of these possibilities.

Drug interactions can trigger various neurological side effects, including headaches, fatigue, muscle weakness, and confusion.

Drug-drug interactions occur when two or more drugs interact within the body, affecting each other's actions. This can involve altering absorption, metabolism, or elimination, potentially causing adverse effects.

Digoxin inhibits the sodium-potassium pump in heart cells, causing increased intracellular sodium. This, in turn, reduces calcium extrusion and increases calcium levels within the cell, enhancing myocardial contractility.

Digoxin is used as a second-line treatment for heart failure, especially in patients with atrial fibrillation. It can improve heart function, but its effectiveness is limited, with only about 50% of patients experiencing relief.

Digoxin can be used to treat irregular heart rhythms (arrhythmias) by influencing the electrical properties of the heart. It slows the rate of electrical impulses from the atria to the ventricles, helping to regulate the heartbeat.

Digoxin has a narrow therapeutic index, meaning the difference between a therapeutic dose and a toxic dose is small. This requires careful monitoring of blood levels.

Digoxin accumulates in the body, making toxicity a concern, especially with long-term use. Early signs include nausea, vomiting, and diarrhea, but more severe symptoms can involve irregular heartbeat.