Angina Medication: Treatment Options for Chest Pain

What Is Angina and Why Does It Need Treatment?

Angina pectoris is chest pain or discomfort caused when the heart muscle doesn't receive enough oxygen-rich blood. It occurs when coronary arteries are narrowed by atherosclerosis. Medications treat angina by reducing the heart's oxygen demand, dilating blood vessels, and preventing blood clots that could cause a heart attack.

Angina affects over 100 million people worldwide and is a major warning sign of coronary artery disease (CAD). The condition develops when fatty plaques build up in the coronary arteries, restricting blood flow to the heart muscle. During physical exertion or emotional stress, the heart requires more oxygen than the narrowed arteries can deliver, resulting in the characteristic chest pain, pressure, or tightness that defines angina.

Understanding why angina occurs is crucial for comprehending how medications work. The heart is a muscular pump that requires a constant supply of oxygenated blood to function properly. When coronary arteries become narrowed by 50% or more, blood flow during periods of increased demand becomes insufficient. This oxygen shortage triggers pain signals that the brain interprets as chest discomfort. The pain typically subsides with rest as oxygen demand decreases, but without treatment, the underlying disease continues to progress.

The goals of angina medication extend beyond simply relieving chest pain. A comprehensive treatment strategy aims to reduce the frequency and severity of angina episodes, improve exercise capacity and quality of life, slow the progression of underlying coronary artery disease, and most importantly, reduce the risk of heart attack and death. Achieving these goals typically requires multiple medications working through different mechanisms.

Types of Angina

Understanding the type of angina helps guide medication selection. Stable angina follows a predictable pattern, occurring during physical activity or stress and relieved by rest or nitroglycerin. Unstable angina is more dangerous, occurring unpredictably, at rest, or with increasing frequency, and requires immediate medical attention. Variant (Prinzmetal) angina results from coronary artery spasm rather than fixed narrowing and often occurs at rest, particularly at night.

Each type of angina may respond differently to various medications. Stable angina typically responds well to standard anti-anginal therapy, while variant angina often requires calcium channel blockers that prevent arterial spasm. Unstable angina is a medical emergency that may require hospitalization and more aggressive treatment, including antiplatelet therapy and possible coronary intervention.

How Do Nitrates Work for Angina?

Nitrates are the most effective medications for rapid angina relief. They work by dilating blood vessels, reducing the heart's workload and improving blood flow to the heart muscle. Sublingual nitroglycerin works within 1-3 minutes and remains the essential rescue medication for acute angina attacks. Long-acting nitrates provide ongoing prevention but require a nitrate-free period to maintain effectiveness.

Nitrates have been used to treat angina for over 150 years, making them one of the oldest and most proven cardiovascular medications. Their mechanism of action involves conversion to nitric oxide in the body, which causes smooth muscle relaxation in blood vessel walls. This relaxation affects both veins and arteries, producing beneficial effects that rapidly relieve angina symptoms.

When veins dilate, blood pools in the venous system, reducing the amount of blood returning to the heart (preload). This decreases the volume of blood the heart must pump with each beat, reducing wall stress and oxygen demand. Arterial dilation, particularly of the coronary arteries, improves blood flow directly to oxygen-starved heart muscle. The combination of reduced demand and improved supply quickly alleviates angina.

Nitrates also have effects that extend beyond immediate symptom relief. They reduce the tendency for coronary artery spasm, which can trigger angina in some patients. Additionally, nitrates may improve blood flow to areas of the heart that are partially blocked, helping to protect heart muscle during periods of ischemia.

Short-Acting Nitroglycerin

Sublingual nitroglycerin tablets or spray should be carried by every angina patient. When placed under the tongue at the first sign of chest discomfort, the medication is absorbed directly into the bloodstream, bypassing the digestive system for rapid effect. Most patients experience relief within 1-3 minutes, though some may need a second or third dose at 5-minute intervals.

Using nitroglycerin correctly is essential for maximum benefit. The medication should be taken while seated to prevent falls from blood pressure drops. Patients should not swallow the tablet but let it dissolve completely under the tongue. A burning or tingling sensation under the tongue indicates an active medication. If chest pain persists after three doses over 15 minutes, emergency medical services should be contacted immediately, as this may indicate a heart attack.

Nitroglycerin tablets are sensitive to heat, light, and moisture, which can reduce their potency. Patients should replace their supply every 6 months and store tablets in their original glass container. Nitroglycerin spray is more stable and doesn't require replacement as frequently, making it a convenient alternative for some patients.

Long-Acting Nitrates

For patients with frequent angina episodes, long-acting nitrates such as isosorbide mononitrate (ISMN) or isosorbide dinitrate (ISDN) provide sustained prevention. These oral medications work through the same mechanism as nitroglycerin but are formulated for gradual absorption and prolonged effect. They are typically taken once or twice daily to reduce the frequency of angina attacks.

A critical consideration with long-acting nitrates is the development of tolerance. When nitrate levels remain constant in the blood, the body's response diminishes over time, reducing effectiveness. To prevent tolerance, doctors prescribe dosing schedules that include a nitrate-free period of 10-14 hours each day. For example, isosorbide mononitrate extended-release is taken once in the morning, leaving the evening and night as a nitrate-free interval.

Transdermal nitroglycerin patches offer another option for continuous prevention. Applied to the skin, these patches deliver a steady dose of nitroglycerin over 12-14 hours. They must be removed at night to maintain a nitrate-free period and prevent tolerance development.

What Are Beta-Blockers and Why Are They First-Line Treatment?

Beta-blockers are typically the first-choice medication for preventing angina episodes. By blocking the effects of adrenaline on the heart, they slow heart rate and reduce blood pressure, decreasing the heart's oxygen demand. Clinical trials show beta-blockers reduce mortality by 20-30% in patients with coronary artery disease. Common examples include metoprolol, bisoprolol, and atenolol.

Beta-blockers represent a cornerstone of angina treatment and have been proven in numerous clinical trials to improve outcomes in patients with coronary artery disease. These medications work by blocking beta-adrenergic receptors in the heart, which normally respond to stress hormones like adrenaline (epinephrine) and noradrenaline (norepinephrine). When these receptors are blocked, the heart beats more slowly and with less force, reducing its oxygen requirements.

The benefits of beta-blockers extend well beyond symptom relief. By reducing heart rate and blood pressure, these medications decrease the stress on coronary artery plaques, making rupture and subsequent heart attack less likely. Beta-blockers also improve the heart's efficiency during exercise, allowing patients to be more active before experiencing angina symptoms. In patients who have previously suffered a heart attack, beta-blockers significantly reduce the risk of sudden cardiac death.

Different beta-blockers have varying properties that influence their selection for individual patients. Cardioselective beta-blockers such as metoprolol, bisoprolol, and atenolol primarily affect the heart, making them preferred choices for patients with asthma or peripheral vascular disease who might not tolerate non-selective agents. Non-selective beta-blockers like propranolol block receptors throughout the body and may cause bronchospasm or worsen circulation problems in susceptible individuals.

How Beta-Blockers Reduce Angina

Beta-blockers address angina through multiple mechanisms that collectively reduce myocardial oxygen demand. The reduction in heart rate is particularly important because the heart uses the most oxygen during the contraction phase. By slowing the heart, beta-blockers increase the time the heart spends in diastole (the relaxation phase), which is when coronary blood flow primarily occurs. This improves the supply-demand balance that is disrupted in angina.

Blood pressure reduction also plays a role. When the heart must pump against lower resistance, it requires less energy and therefore less oxygen. Beta-blockers reduce blood pressure through several mechanisms, including decreased heart output and reduced release of renin from the kidneys, which affects fluid balance and vascular tone.

Additionally, beta-blockers reduce the heart's contractile force. While this might seem counterproductive, the energy savings from less forceful contractions outweigh any reduction in pumping efficiency, particularly in patients with adequate baseline heart function. For patients with heart failure, certain beta-blockers have been shown to actually improve heart function over time by protecting against the damaging effects of chronic stress hormone activation.

Starting and Adjusting Beta-Blocker Therapy

Beta-blockers are typically started at low doses and gradually increased to achieve target heart rate and blood pressure goals. The target resting heart rate for angina patients is generally 55-60 beats per minute, low enough to reduce oxygen demand but not so low as to cause symptoms like fatigue or dizziness. Blood pressure goals depend on individual factors but typically aim for less than 130/80 mmHg.

Common side effects during initiation include fatigue, cold extremities, and sometimes depression or sleep disturbances. Many patients find these effects diminish over time as the body adjusts. Weight gain can occur due to mild metabolic effects, and patients with diabetes should monitor blood glucose more carefully as beta-blockers can mask hypoglycemia symptoms and affect insulin sensitivity.

How Do Calcium Channel Blockers Help Angina?

Calcium channel blockers (CCBs) are effective angina medications that work by relaxing blood vessels and reducing heart contractility. They are particularly useful for variant (Prinzmetal) angina caused by coronary artery spasm. There are two main types: dihydropyridines (like amlodipine) primarily dilate blood vessels, while non-dihydropyridines (diltiazem, verapamil) also slow heart rate. CCBs can be used alone or combined with beta-blockers for enhanced effect.

Calcium channel blockers represent another major class of anti-anginal medications with mechanisms that complement those of beta-blockers and nitrates. These drugs work by blocking voltage-gated calcium channels in cardiac muscle and smooth muscle cells. Calcium is essential for muscle contraction, so blocking its entry causes relaxation. The resulting effects include vasodilation (widening of blood vessels), reduced heart muscle contractility, and in some CCBs, slowed heart rate.

The two main categories of calcium channel blockers have distinct properties that determine their clinical use. Dihydropyridine CCBs such as amlodipine, nifedipine, and felodipine primarily affect blood vessel smooth muscle, causing significant vasodilation with minimal direct effect on the heart. This makes them excellent choices for reducing blood pressure and improving coronary blood flow. Non-dihydropyridine CCBs like diltiazem and verapamil also affect the heart directly, slowing heart rate and reducing contractility similar to beta-blockers.

The choice between these subclasses depends on individual patient characteristics. Patients with rapid heart rates may benefit from the rate-slowing effects of diltiazem or verapamil. Those who cannot tolerate beta-blockers due to asthma or other conditions often do well with non-dihydropyridine CCBs as an alternative. Dihydropyridine CCBs like amlodipine are frequently combined with beta-blockers since they work through complementary mechanisms without excessively slowing heart rate.

Calcium Channel Blockers for Variant Angina

Calcium channel blockers are particularly effective for variant (Prinzmetal) angina, a form of angina caused by coronary artery spasm rather than fixed atherosclerotic narrowing. In these patients, the coronary arteries temporarily constrict, dramatically reducing blood flow to the heart muscle. CCBs prevent this spasm by blocking the calcium-dependent contraction of coronary artery smooth muscle.

Patients with variant angina often experience chest pain at rest, frequently at night or in the early morning hours. The attacks may occur in cycles, with periods of frequent symptoms followed by symptom-free intervals. While nitroglycerin can relieve acute episodes, calcium channel blockers are the mainstay of preventive treatment, often providing dramatic improvement in symptom frequency and severity.

Combining Calcium Channel Blockers with Other Medications

When angina is inadequately controlled with a single medication, combining different drug classes often provides better symptom relief. Dihydropyridine CCBs like amlodipine combine well with beta-blockers because they have complementary mechanisms—the CCB provides vasodilation while the beta-blocker controls heart rate. This combination is widely used and generally well-tolerated.

Combining non-dihydropyridine CCBs (diltiazem, verapamil) with beta-blockers requires more caution because both slow heart rate. This combination may cause excessive bradycardia (slow heart rate) or heart block in susceptible patients. When used together, careful monitoring and lower doses of each medication are typically needed.

Why Is Aspirin Essential for Angina Patients?

Aspirin is a critical medication for angina patients because it prevents blood clots that can cause heart attacks. By inhibiting platelet aggregation, low-dose aspirin (75-100mg daily) reduces the risk of myocardial infarction by 25-30%. Nearly all angina patients should take aspirin unless they have a specific contraindication such as active bleeding or aspirin allergy. Aspirin is one of the most cost-effective treatments for preventing cardiovascular events.

While anti-anginal medications like nitrates and beta-blockers focus on symptom relief and prevention, aspirin addresses a different but equally important goal: preventing the heart attacks that claim many angina patients' lives. Angina occurs because coronary arteries are narrowed by atherosclerotic plaques. These plaques can suddenly rupture, triggering rapid blood clot formation that completely blocks the artery and causes a heart attack. Aspirin helps prevent this catastrophic event.

Aspirin works by irreversibly inhibiting cyclooxygenase-1 (COX-1) enzyme in platelets, preventing the production of thromboxane A2, a powerful promoter of platelet aggregation and vasoconstriction. Because platelets cannot synthesize new enzymes, a single dose of aspirin inhibits platelet function for the entire 7-10 day lifespan of the platelet. This explains why even low doses taken once daily provide continuous antiplatelet protection.

The evidence supporting aspirin use in coronary artery disease is extensive and compelling. Multiple large randomized trials and meta-analyses have demonstrated that low-dose aspirin reduces the risk of heart attack by 25-30% in patients with established cardiovascular disease. This benefit far outweighs the small increased risk of bleeding complications in most patients.

Appropriate Aspirin Dosing

The optimal dose of aspirin for cardiovascular prevention has been extensively studied. Current guidelines recommend low-dose aspirin, typically 75-100mg daily, for secondary prevention in patients with established cardiovascular disease including angina. Lower doses are as effective as higher doses for preventing cardiovascular events while causing fewer gastrointestinal side effects.

Enteric-coated or buffered aspirin formulations may reduce stomach irritation but do not eliminate bleeding risk, which occurs through systemic rather than local effects. Patients with a history of gastric ulcers or bleeding may need concurrent proton pump inhibitor (PPI) therapy to protect the stomach lining while continuing aspirin therapy.

When Aspirin Should Be Avoided

Despite its benefits, aspirin is not appropriate for everyone. Contraindications include active gastrointestinal bleeding, aspirin allergy (which can cause severe anaphylaxis), bleeding disorders, and recent hemorrhagic stroke. Patients taking anticoagulants like warfarin or direct oral anticoagulants require careful assessment of bleeding risk before adding aspirin.

For patients who cannot take aspirin, clopidogrel (Plavix) is an alternative antiplatelet agent that works through a different mechanism. Clopidogrel inhibits the P2Y12 adenosine diphosphate receptor on platelets, preventing their activation and aggregation. While effective, clopidogrel is more expensive than aspirin and may be reserved for patients with true aspirin intolerance.

How Do Statins Protect the Heart in Angina?

Statins are essential medications for angina patients because they stabilize arterial plaques and reduce cardiovascular events beyond their cholesterol-lowering effects. High-intensity statin therapy reduces LDL cholesterol by 50% or more and decreases heart attack and stroke risk by about 25-35%. Current guidelines recommend high-intensity statins for all patients with established coronary artery disease, regardless of baseline cholesterol levels.

Statins have revolutionized the treatment of cardiovascular disease since their introduction in the 1980s. While initially developed to lower cholesterol, research has revealed that their benefits extend far beyond lipid reduction. Statins stabilize vulnerable plaques, reduce inflammation, improve endothelial function, and decrease the likelihood of plaque rupture and subsequent heart attack. These pleiotropic effects make statins essential for virtually all angina patients.

The mechanism of action involves inhibition of HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis. When cholesterol production in the liver decreases, cells increase their expression of LDL receptors, pulling more LDL cholesterol out of the bloodstream. The result is substantial reductions in LDL cholesterol, often by 50% or more with high-intensity statins.

For patients with established coronary artery disease, including those with angina, guidelines recommend high-intensity statin therapy to achieve an LDL cholesterol target of less than 70 mg/dL (1.8 mmol/L). High-intensity statins include atorvastatin 40-80mg and rosuvastatin 20-40mg daily. These doses provide the greatest reduction in cardiovascular events based on large clinical trials.

Benefits Beyond Cholesterol Reduction

The cardiovascular benefits of statins are partially independent of their cholesterol-lowering effects, a phenomenon that has generated considerable research interest. Statins reduce inflammatory markers like C-reactive protein (CRP), which may reflect reduced arterial inflammation. They improve endothelial function, enhancing the ability of blood vessels to dilate and respond to changes in blood flow.

Perhaps most importantly for angina patients, statins appear to stabilize atherosclerotic plaques. Vulnerable plaques with thin fibrous caps and large lipid cores are most likely to rupture and cause heart attacks. Statins thicken the fibrous cap, reduce lipid content, and decrease the macrophages and inflammatory cells that weaken plaque structure. This plaque stabilization may explain why statin benefits appear quickly after starting treatment, before maximum cholesterol reduction is achieved.

Common Statin Side Effects

While statins are generally well-tolerated, some patients experience side effects that may require dose adjustment or medication switching. Muscle symptoms are the most common complaint, ranging from mild aching to rare but serious muscle breakdown (rhabdomyolysis). True statin-related myopathy occurs in about 1-5% of patients, and many patients who initially attribute muscle symptoms to statins can tolerate the same medication in rechallenge studies.

Other potential side effects include liver enzyme elevations (usually mild and transient), increased risk of diabetes (particularly in those already at high risk), and occasionally gastrointestinal symptoms. The cardiovascular benefits of statins substantially outweigh these risks for patients with established coronary artery disease, but each patient should discuss the risk-benefit balance with their healthcare provider.

What Are Newer Medications for Angina?

When traditional angina medications are insufficient or not tolerated, newer agents like ranolazine, ivabradine, and nicorandil offer additional treatment options. Ranolazine works through a unique mechanism to reduce angina without affecting heart rate or blood pressure. Ivabradine specifically slows heart rate and may benefit patients who cannot tolerate beta-blockers. These medications are typically added to standard therapy for refractory angina.

Despite optimal therapy with nitrates, beta-blockers, calcium channel blockers, and risk-modifying medications, some patients continue to experience angina. For these individuals, newer medications with different mechanisms of action may provide additional benefit. These agents represent important additions to the angina treatment toolkit, offering options when traditional therapies fail or are not tolerated.

Ranolazine

Ranolazine is a unique anti-anginal medication that works by inhibiting the late sodium current in cardiac cells. During ischemia, sodium accumulates inside heart cells, leading to calcium overload and impaired relaxation. By reducing this sodium accumulation, ranolazine improves myocardial relaxation and reduces oxygen consumption. Importantly, ranolazine does not significantly affect heart rate or blood pressure, making it well-suited for addition to other medications.

Clinical trials have shown that ranolazine reduces angina frequency and improves exercise capacity when added to standard anti-anginal therapy. It is particularly useful in patients with diabetes, as it does not worsen glycemic control and may actually improve HbA1c levels. Common side effects include constipation, dizziness, and nausea. Ranolazine can prolong the QT interval on electrocardiogram and should be avoided in patients with pre-existing QT prolongation.

Ivabradine

Ivabradine specifically inhibits the If (funny) channel in the sinoatrial node, the heart's natural pacemaker. This reduces heart rate without affecting blood pressure, myocardial contractility, or intracardiac conduction. For patients with angina who have elevated resting heart rates despite beta-blocker therapy, or who cannot tolerate beta-blockers, ivabradine offers an alternative approach to rate control.

By slowing the heart rate, ivabradine reduces myocardial oxygen demand and increases diastolic filling time, improving coronary perfusion. Studies have shown improved exercise capacity and reduced angina symptoms. However, ivabradine should not be used in patients with atrial fibrillation, as its mechanism requires normal sinus rhythm. Visual disturbances (luminous phenomena) are a distinctive side effect that usually resolves with continued use.

Nicorandil

Nicorandil combines two mechanisms: nitrate-like action that dilates veins and coronary arteries, and potassium channel activation that dilates arterioles. This dual action reduces both preload and afterload while improving coronary blood flow. Nicorandil has been shown to reduce cardiovascular events in patients with stable angina in some studies, though it is not available in all countries.

Side effects of nicorandil include headache (similar to nitrates), flushing, and rarely, gastrointestinal or mucosal ulceration. The medication should be used with caution in patients already taking nitrates or phosphodiesterase-5 inhibitors due to the risk of excessive blood pressure reduction.

How Are Angina Medications Combined?

Most angina patients require multiple medications for optimal control. A typical regimen includes a beta-blocker for prevention, sublingual nitroglycerin for acute episodes, aspirin for heart attack prevention, and a high-intensity statin for risk reduction. Additional agents like calcium channel blockers or ranolazine may be added if symptoms persist. Each medication class addresses different aspects of angina management.

Effective angina treatment typically involves a multi-pronged approach using medications with complementary mechanisms. This strategy maximizes symptom relief while addressing the underlying disease and reducing long-term cardiovascular risk. Understanding how these medications work together helps patients appreciate why their treatment regimen may include multiple drugs.

Building an Optimal Medication Regimen

The foundation of angina treatment typically begins with a beta-blocker for symptom prevention and mortality reduction. All patients should have sublingual nitroglycerin available for acute episodes, regardless of how well-controlled their symptoms appear. Aspirin (unless contraindicated) and a high-intensity statin are added for secondary prevention of cardiovascular events.

If angina persists despite beta-blocker therapy, a dihydropyridine calcium channel blocker like amlodipine is often added. This combination is synergistic, with the CCB providing additional vasodilation while the beta-blocker prevents reflex tachycardia. For patients who cannot tolerate beta-blockers, a non-dihydropyridine CCB (diltiazem or verapamil) may serve as the primary rate-controlling agent.

When symptoms remain problematic despite dual anti-anginal therapy, ranolazine offers a third-line option that can be safely combined with existing medications. Long-acting nitrates may be added for additional preventive effect, though tolerance must be considered when designing the dosing schedule.

How Do Lifestyle Changes Work with Medications?

Lifestyle modifications are essential partners to medication therapy in angina treatment. Smoking cessation alone can halve the risk of future cardiovascular events. Regular exercise, supervised cardiac rehabilitation, heart-healthy diet, and weight management can reduce angina symptoms by 50% or more. These changes work synergistically with medications but should never replace them without medical guidance.

While medications are indispensable for angina treatment, lifestyle modifications provide complementary benefits that can dramatically improve outcomes. In fact, comprehensive lifestyle changes address the root causes of coronary artery disease and can slow or even partially reverse atherosclerotic plaque development. Patients who combine optimal medical therapy with lifestyle modifications achieve the best long-term results.

Smoking Cessation

For smokers with angina, quitting tobacco is the single most important lifestyle change. Smoking accelerates atherosclerosis, promotes arterial spasm, reduces oxygen-carrying capacity of the blood, and increases clotting tendency. Within one year of quitting, cardiovascular risk decreases by 50%. Various aids including nicotine replacement, bupropion, and varenicline can help with cessation, and healthcare providers should offer ongoing support.

Exercise and Cardiac Rehabilitation

Regular physical activity improves cardiovascular fitness, reduces symptoms, and decreases mortality in angina patients. However, exercise must be approached carefully, as it can trigger angina in patients with significant coronary disease. Cardiac rehabilitation programs provide supervised exercise with appropriate monitoring, gradually increasing intensity as fitness improves. Studies show cardiac rehabilitation can reduce cardiovascular mortality by 20-30%.

Patients should work with their healthcare team to develop an exercise plan that balances benefit with safety. This typically involves starting with low-intensity activities and gradually progressing based on symptom response. Having nitroglycerin available during exercise and knowing warning signs that require stopping activity are essential safety measures.

Diet and Weight Management

A heart-healthy diet reduces cholesterol, blood pressure, and inflammation while helping achieve healthy weight. The Mediterranean diet, rich in vegetables, fruits, whole grains, fish, and olive oil with limited red meat and processed foods, has the strongest evidence for cardiovascular protection. Reducing sodium intake helps control blood pressure, while limiting saturated and trans fats improves lipid profiles.

Weight loss in overweight patients reduces the heart's workload and can improve angina symptoms. Even modest weight loss of 5-10% of body weight can produce meaningful improvements in cardiovascular risk factors including blood pressure, blood sugar, and cholesterol levels.

When Should You Seek Emergency Care for Angina?

Seek emergency medical care immediately if chest pain is severe, lasts more than 15 minutes, or is not relieved by 3 doses of nitroglycerin. Other warning signs requiring immediate attention include chest pain at rest, pain spreading to arms/jaw/back, shortness of breath, sweating, or nausea. These symptoms may indicate a heart attack, which requires urgent treatment to prevent permanent heart damage.

Understanding when angina symptoms require emergency care is critical for all angina patients. While stable angina follows a predictable pattern and responds to nitroglycerin, certain presentations suggest a heart attack in progress and require immediate intervention. Delays in treatment can result in permanent heart muscle damage or death.

Unstable angina represents a dangerous transition between stable disease and heart attack. Unlike stable angina, unstable angina may occur at rest, wake patients from sleep, or be triggered by minimal exertion. The pattern changes, with episodes becoming more frequent, more severe, or lasting longer. Any change in the usual pattern of angina warrants prompt medical evaluation, even if symptoms resolve with nitroglycerin.

Patients experiencing a heart attack may describe symptoms differently from their usual angina. The pain may be more intense, may not respond to nitroglycerin, and may be accompanied by symptoms like profuse sweating, nausea, shortness of breath, or a sense of impending doom. However, some heart attacks produce only mild symptoms, particularly in women, diabetics, and elderly patients. When in doubt, it is always safer to seek emergency evaluation.