Angina pectoris - causes, Symptoms, Treatment

When your heart muscle (myocardium) does not receive enough blood and oxygen for the amount of work being done, angina pectoris develops. A condition called ischemia occurs when there is insufficient blood flow.

Angina can be brought on by anything that makes your heart muscle require extra blood or oxygen. Physical activity, emotional stress, extreme cold or heat, heavy meals, excessive alcohol consumption, and cigarette smoking are risk factors.

Doctor may run blood tests, an electrocardiogram (ECG), or a stress test without imaging to diagnose your illness. Also possible are chest x-rays, chest CTs, coronary CT angiograms, cardiac MRIs, coronary angiograms, echocardiograms, and stress tests with imaging.

The presence of angina indicates the presence of coronary artery disease and a lack of blood flow to a portion of the heart. You run a higher risk of having a heart attack if you have angina.

Angina, however, is not an illness. It is a symptom of a cardiac ailment that is already present, often coronary heart disease (CHD), also referred to as coronary artery disease (CAD).

Angina pectoris is chest pain or discomfort caused by reduced blood flow to the heart muscle. Unlike a heart attack, which involves permanent damage to the heart muscle due to prolonged lack of blood supply, angina is temporary and usually resolves with rest or medication. Angina is a warning sign of coronary artery disease, while a heart attack is an acute event.

Angina equivalents are symptoms that may indicate myocardial ischemia (reduced blood flow to the heart) but do not present as typical chest pain. These can include shortness of breath, fatigue, nausea, or sweating, especially during exertion. Recognizing angina equivalents is crucial because they may be the primary symptom in some patients, particularly in women, older adults, and those with diabetes. Failure to identify these symptoms as potential indicators of coronary artery disease can lead to delayed diagnosis and treatment.

Diabetic autonomic neuropathy is a concern in the context of angina and heart disease because it can affect the nerves that control heart rate and blood pressure. This neuropathy can lead to "silent" ischemia, where individuals do not feel the typical chest pain of angina despite reduced blood flow to the heart. The absence of warning symptoms can result in delayed diagnosis and treatment of coronary artery disease. Additionally, autonomic dysfunction can impair the heart's ability to respond appropriately to stress or exercise, potentially exacerbating ischemia and increasing the risk of cardiac events.

Microvascular angina, also known as cardiac syndrome X, differs from traditional angina pectoris in that it involves dysfunction of the small coronary blood vessels rather than blockages in the large coronary arteries. In microvascular angina, these small vessels fail to dilate properly, leading to reduced blood flow to the heart muscle. This condition is more common in women and can be challenging to diagnose because standard coronary angiography may show normal-appearing large coronary arteries.

Coronary collateral circulation refers to alternative blood vessels that can supply blood to heart muscle when the original blood vessels are blocked. In the context of angina, well-developed collateral circulation can significantly influence both severity and prognosis. Patients with good collaterals may experience less severe angina or even be asymptomatic despite significant coronary artery blockages. This is because collaterals provide alternative routes for blood flow, improving oxygen supply to the heart muscle. The presence of robust collateral circulation is generally associated with better outcomes in coronary artery disease, potentially reducing the risk of heart attacks and improving survival rates.

Sleep apnea can significantly interact with and exacerbate angina through several mechanisms. During apneic episodes, oxygen levels in the blood drop, which can trigger or worsen myocardial ischemia in patients with coronary artery disease. The repeated cycles of low oxygen (hypoxia) and reoxygenation can increase oxidative stress and inflammation, contributing to endothelial dysfunction and progression of atherosclerosis. Sleep apnea also activates the sympathetic nervous system, leading to increases in heart rate and blood pressure, which can further strain the heart. Additionally, the fragmented sleep and daytime fatigue associated with sleep apnea can indirectly worsen cardiovascular health by promoting sedentary behavior and making exercise more challenging. Recognizing and treating sleep apnea in patients with angina is crucial for comprehensive cardiovascular care.

Atherosclerosis contributes to angina pectoris by causing the buildup of plaque in the coronary arteries. This plaque narrows the arteries, reducing blood flow to the heart muscle. As the arteries become more constricted, the heart receives less oxygen-rich blood, especially during times of increased demand, leading to the chest pain characteristic of angina.

Risk factors such as smoking, high blood pressure, and high cholesterol contribute to the development of atherosclerosis, which narrows coronary arteries. Smoking damages blood vessel walls and promotes plaque formation. High blood pressure increases stress on artery walls, while high cholesterol leads to plaque buildup. These factors collectively increase the risk of developing coronary artery disease and, consequently, angina.

Chronic inflammation plays a crucial role in the pathophysiology of angina and atherosclerosis. Inflammation contributes to all stages of atherosclerosis, from initial endothelial dysfunction to plaque formation and rupture. Inflammatory cells like macrophages infiltrate the arterial wall, promoting the oxidation of LDL cholesterol and the formation of foam cells. Inflammatory mediators also stimulate smooth muscle cell proliferation and migration, leading to plaque growth. Chronic inflammation can destabilize plaques, making them more prone to rupture, which can cause acute coronary events. In the context of angina, inflammation can exacerbate arterial narrowing and reduce the flexibility of blood vessels, further compromising blood flow to the heart muscle.

Chronic kidney disease (CKD) significantly impacts both the risk and management of angina. CKD accelerates atherosclerosis and increases cardiovascular risk factors like hypertension and anemia, making angina more likely. Management is complicated because many standard angina medications are cleared by the kidneys and may require dose adjustments. Additionally, CKD patients often have reduced kidney function, limiting the use of contrast agents in diagnostic procedures like angiography. This complex interplay necessitates a carefully tailored approach to angina management in CKD patients.

Angina can be more severe in cold weather due to several factors. Cold temperatures cause blood vessels to constrict, including coronary arteries, which reduces blood flow to the heart. Additionally, cold air can irritate airways, leading to increased respiratory effort and oxygen demand. The body also expends more energy to maintain core temperature in cold conditions. These factors collectively increase the heart's workload and oxygen demand, potentially triggering or exacerbating angina symptoms in susceptible individuals.

Angina is often described as a squeezing or pressure sensation because it results from ischemia (reduced blood flow) to the heart muscle, not direct tissue damage. This type of discomfort is characteristic of visceral pain, which is typically perceived as a diffuse, hard-to-localize sensation rather than a sharp, localized pain.

Angina occurs during physical exertion or emotional stress because these situations increase the heart's demand for oxygen. When coronary arteries are narrowed due to atherosclerosis, they cannot supply enough oxygenated blood to meet the increased demand, resulting in chest pain. This mismatch between oxygen supply and demand triggers angina symptoms.

Referred pain is common in angina because the heart and other thoracic organs share nerve pathways to the spinal cord. The brain may misinterpret the origin of these signals, causing pain to be felt in other areas. Typical sites of referred angina pain include the left arm, jaw, neck, back, and sometimes the right arm. This phenomenon is due to the convergence of sensory neurons from different body regions in the spinal cord.

Silent ischemia refers to episodes of reduced blood flow to the heart that do not cause noticeable symptoms. Unlike typical angina, which causes chest pain or discomfort, silent ischemia occurs without warning. It's concerning because it can cause heart damage without the person being aware, potentially leading to a heart attack or other serious cardiac events without preceding symptoms that might prompt medical attention.

The autonomic nervous system influences angina symptoms through its regulation of heart rate and blood vessel constriction. Sympathetic nervous system activation during stress can increase heart rate and constrict blood vessels, potentially triggering or worsening angina. Conversely, parasympathetic activation can help alleviate symptoms by slowing heart rate and promoting relaxation.

Nitroglycerin works by dilating blood vessels, including coronary arteries. This dilation increases blood flow to the heart muscle and reduces the workload on the heart. By improving the balance between oxygen supply and demand in the heart, nitroglycerin quickly relieves angina symptoms.

Beta-blockers help treat angina by blocking the effects of adrenaline and other stress hormones on the heart. This action reduces heart rate, blood pressure, and the heart's workload, thereby decreasing oxygen demand. By improving the balance between oxygen supply and demand, beta-blockers can prevent or reduce the frequency and severity of angina episodes, especially during physical or emotional stress.

Exercise can trigger angina by increasing the heart's oxygen demand, which may exceed the supply in patients with coronary artery disease. However, regular exercise is also recommended for stable angina patients because it promotes cardiovascular health. Exercise training can improve the heart's efficiency, enhance coronary blood flow, reduce risk factors like obesity and high blood pressure, and even stimulate the growth of new blood vessels (collateral circulation). This paradox highlights the importance of properly supervised and gradually increased exercise programs for angina patients.

Angina and heart rhythm disturbances are often interrelated. Reduced blood flow to the heart during an angina episode can trigger arrhythmias by disrupting the heart's electrical system. Conversely, certain arrhythmias can increase the heart's workload or decrease its efficiency, potentially triggering or worsening angina symptoms. This bidirectional relationship underscores the importance of managing both conditions in patients with heart disease.

Ischemic preconditioning refers to the phenomenon where brief, non-lethal episodes of ischemia (reduced blood flow) can protect the heart against subsequent, more severe ischemic events. In the context of angina, repeated mild angina episodes may actually condition the heart to better tolerate future ischemic stress. This adaptation involves complex cellular mechanisms that enhance the heart's resilience to oxygen deprivation, potentially reducing the severity of future angina episodes or even offering some protection against heart attacks.

Stable angina occurs predictably, usually triggered by specific activities or stress, and is relieved by rest or medication. Unstable angina is more severe, occurs unpredictably, may happen at rest, and doesn't respond as well to treatment. Unstable angina is considered a medical emergency as it may indicate an impending heart attack.

Coronary artery spasm, also known as vasospastic or Prinzmetal's angina, occurs when a coronary artery temporarily constricts, reducing blood flow to the heart. Unlike atherosclerotic angina, which is caused by fixed narrowing of arteries, vasospastic angina can occur in people with or without significant coronary artery disease. It often happens at rest, particularly in the early morning, and can be triggered by factors like stress, cold, or certain medications.

Variant angina, or Prinzmetal's angina, challenges the traditional understanding of angina triggers because it typically occurs at rest, often during sleep or in the early morning, rather than during exertion. This condition is caused by spasms of the coronary arteries rather than fixed atherosclerotic narrowing. It demonstrates that angina can result from dynamic changes in coronary artery tone, not just from increased oxygen demand or fixed arterial obstruction. This understanding has important implications for diagnosis and treatment, as variant angina may require different management strategies compared to typical exertional angina.

Crescendo angina refers to a pattern of increasingly frequent, severe, or prolonged angina episodes over a short period, typically days or weeks. It's considered a medical emergency because it often signals a critical progression of coronary artery disease and a high risk of impending heart attack. Crescendo angina suggests that atherosclerotic plaques may be becoming unstable or that coronary artery narrowing is rapidly worsening. This pattern indicates a transition from stable to unstable angina and requires immediate medical attention to prevent myocardial infarction. The urgency stems from the need to stabilize the coronary situation, often through interventions like angioplasty or coronary bypass surgery, to prevent potentially life-threatening complications.

Angina decubitus refers to angina that occurs when lying down, typically shortly after going to bed. This type of angina is significant because it often indicates advanced coronary artery disease or heart failure. When a person lies flat, venous return to the heart increases, which can raise the pressure within the heart chambers. In patients with compromised heart function, this increased pressure can lead to pulmonary congestion and reduced coronary perfusion, triggering angina. The presence of angina decubitus suggests a need for careful evaluation of overall cardiac function and may indicate a need for more aggressive treatment of underlying heart disease.

Myocardial stunning refers to the temporary dysfunction of heart muscle following an episode of ischemia, even after blood flow has been restored. In the context of angina, repeated episodes of ischemia can lead to cumulative stunning effects, where portions of the heart muscle function suboptimally even when not actively experiencing angina. This phenomenon has implications for overall heart function and can contribute to the progression of heart failure in some patients with chronic angina. Understanding myocardial stunning emphasizes the importance of preventing recurrent angina episodes to preserve long-term heart function.

"Walk-through angina" refers to the phenomenon where angina pain that occurs at the beginning of exercise subsides as the activity continues. This occurs because initial exertion increases oxygen demand, causing angina, but as exercise persists, the coronary arteries dilate and collateral blood vessels open up, improving blood flow to the heart muscle. This phenomenon indicates the heart's ability to adapt to ischemic conditions through mechanisms like coronary vasodilation and recruitment of collateral circulation, highlighting the dynamic nature of coronary blood flow regulation.

The "warm-up phenomenon" in angina refers to the observation that some patients experience less angina with continued or repeated exercise. After an initial bout of angina during exertion, subsequent similar levels of exertion may not provoke symptoms or may cause less severe symptoms. This phenomenon demonstrates the heart's remarkable adaptive capabilities. It's thought to occur due to several mechanisms, including improved coronary blood flow through dilation of blood vessels, enhanced oxygen utilization by the heart muscle, and possibly ischemic preconditioning effects. The warm-up phenomenon highlights the dynamic nature of the heart's response to stress and the potential benefits of properly structured exercise programs in managing stable angina.

The "ischemic cascade" refers to the sequence of events that occur in the heart muscle during an episode of reduced blood flow (ischemia). Understanding this cascade is crucial for comprehending the progression of an angina episode. The sequence typically follows this order: