Angina pectoris
Call 9-1-1 immediately: signs of a possible acute coronary syndrome
Chest pain at rest, new or unusual, lasting more than 20 minutes Any chest pain occurring without exertion, especially at night or at rest, in a patient with or without known angina, should be considered an acute coronary syndrome (unstable angina or myocardial infarction) until proven otherwise. Do not drive yourself. Call 911.
Recent change in angina pattern Increased frequency of seizures, triggering with less effort than before, more intense or prolonged pain, onset of seizures at rest in a usually stable patient. These changes define de novo or crescendo unstable angina, which requires urgent evaluation in a hospital setting on the same day.
Chest pain not relieved by two or three doses of sublingual nitroglycerin at 5-minute intervals The absence of relief with sublingual nitro after a total of 15 minutes is highly suggestive of an ongoing myocardial infarction and warrants an immediate call to 911. Chew one regular strength 325 mg aspirin tablet (or 4 x 81 mg tablets) immediately if available, unless there is a documented allergy.
Chest pain associated with Severe shortness of breath, profuse sweating, paleness, nausea and vomiting, palpitations or fainting, radiating pain to the left arm, jaw, neck, or back. These accompanying vegetative signs greatly increase the probability of an acute myocardial infarction.
First documented anginal attack ever, even subsiding with rest Any chest pain suggestive of angina occurring for the first time without a prior coronary diagnosis must be evaluated urgently in a hospital setting to rule out ACS and establish an etiologic diagnosis.
Pathophysiology of myocardial ischemia
The myocardium is a tissue with a very high metabolic demand for oxygen, functioning almost exclusively aerobically and incapable of sustaining prolonged oxygen debt without contractile dysfunction. Coronary perfusion ensures an oxygen supply closely coupled to myocardial demand through coronary vascular autoregulation mechanisms, the reserve of which is considerable in healthy individuals (coronary flow can be multiplied by 4 to 5 during maximal exertion). Coronary atherosclerosis, through the accumulation of lipid and fibrous plaques in the wall of epicardial coronary arteries, progressively reduces the arterial lumen and limits this coronary vasodilation reserve. When stenosis exceeds 50% to 70% %of the luminal diameter, the coronary reserve is significantly reduced; beyond 70% to 80% % , stenosis can become hemodynamically significant even at rest.
During physical exertion, emotional stress or any condition that increases myocardial oxygen demand (tachycardia, hypertension, increased contractility), coronary flow can no longer increase proportionally downstream of a critical stenosis. The resulting transient tissue ischemia triggers a cascade of metabolic disturbances in the so-called «ischemic cascade» sequence: first a scintigraphic perfusion abnormality, then diastolic dysfunction, then segmental systolic dysfunction, then electrocardiographic abnormalities (ST segment sub-shift), and finally anginal pain, which is therefore the last sign to appear in the ischemic sequence. This hierarchy explains why many ischemic episodes are completely silent (silent ischemia, particularly common in diabetic patients with cardiac vegetative neuropathy), and why myocardial perfusion imaging tests are more sensitive than stress ECG for detecting ischemia.
Beyond obstructive atherosclerosis, other mechanisms can contribute to angina: coronary spasm (Prinzmetal's angina or vasospastic angina, due to sudden and transient contraction of a coronary segment, often in a minimally or non-atherosclerotic artery, triggered by cold, tobacco, cocaine, certain medications, or hyperventilation); coronary microvascular dysfunction (microvascular angina, formerly «cardiac syndrome X,» due to impaired vasodilation reserve of small coronary arterioles without significant epicardial stenosis, more common in women, particularly during the perimenopausal period); and increased myocardial demand without underlying coronary disease (functional angina due to severe anemia, thyrotoxicosis, massive left ventricular hypertrophy, or obstructive cardiomyopathy).
Clinical Presentation of Stable Angina
The classic description of stable angina pectoris, codified since the work of William Heberden in 1768, remains the primary clinical diagnostic reference. Typical angina pain combines three essential semiological features: a retrosternal or precordial location, with possible irradiation into the left arm (medial aspect), lower jaw, neck, left shoulder or both shoulders, and more rarely into the back, right arm or epigastrium; a constrictive, oppressive or vise-like character (the patient often places the closed fist on the sternum, Levine's sign), sometimes described as a heavy, deep burning or choking sensation (the term «angina» derives from the Latin for «strangulation»); triggered by physical exertion, cold, emotional stress or post-prandial digestion (increased cardiac workload), with cession in less than 10 to 15 minutes after cessation of exertion, or after sublingual nitroglycerin in less than 5 minutes.
The presence of three characteristics defines typical angina, with a very high pre-test probability of underlying coronary artery disease. The presence of two characteristics defines atypical angina (intermediate probability). The presence of only one characteristic or none defines non-anginal chest pain (low probability). This Diamond and Forrester classification, incorporated into the European (ESC 2019) and Canadian recommendations, guides the strategy for further investigations based on the pre-test probability of obstructive coronary artery disease, adjusted according to the patient's age and sex.
In women, the clinical presentation of angina is frequently atypical: epigastric pain, unexplained fatigue, exertional dyspnea, nausea, back pain, without the classic retrosternal constrictive pain. This atypicality, associated with a historical tendency for underestimation of cardiovascular risk in women in medical practice, explains why women are often diagnosed and treated later than men for their ischemic heart disease. In diabetic patients, cardiac autonomic neuropathy can completely mask anginal pain, leading to silent ischemia; unexplained exertional dyspnea can be the only manifestation.
Canadian Cardiovascular Society (CCS) classification of angina pectoris
| CCS Class | Functional description | Clinical examples |
|---|---|---|
| Class I | Ordinary physical activity does not cause angina; angina only occurs with intense, prolonged, or rapid exertion. | Angina during sprints, rapid ascent of several floors, intense or unusual physical exertion; no angina for daily living activities |
| Class II | Slight limitation of ordinary physical activity | Angina during brisk walking on level ground, climbing stairs at a normal pace, walking uphill, walking in the cold or after a meal, moderate emotional stress, walking more than two blocks or climbing more than one story at a normal pace |
| Class III | Marked limitation in ordinary physical activity | Angor for any moderate activity: walking one to two blocks on flat terrain, climbing one flight of stairs slowly, dressing and toileting if done quickly |
| 4th Grade | Inability to perform any physical activity without angina; possible angina at rest | Angina for lighter daily activities (dressing, washing), or occurring at rest; clinical overlap with unstable angina; urgent evaluation recommended |
Angor versus acute coronary syndromes: an essential clinical distinction
| Features | Angor Stable | Unstable angina (SCA-NSTEMI) | Myocardial infarction (STEMI) |
|---|---|---|---|
| Pathophysiological mechanism | Fixed coronary stenosis limiting coronary flow reserve during exertion; reversible and transient ischemia | Rupture or erosion of a vulnerable plaque; partial coronary thrombosis; prolonged ischemia | Complete occlusive coronary thrombosis; transmural myocardial necrosis |
| Trigger | Effort, cold, stress, meal; reproducible for a given level of effort | Rest or minimal effort; can occur at night; unpredictable | Often at rest or without a triggering factor; sometimes after intense exertion |
| Duration of pain | Less than 10 to 15 minutes | More than 20 minutes; may be prolonged and recurrent | More than 30 minutes; persistent; does not yield to nitroglycerin |
| Response to nitroglycerin | Onset in less than 5 minutes after sublingual administration | Partial or no relief | Absent, partial, and temporary |
| ECG during the crisis | Transient ST-segment depression on exertion; resting ECG often normal or with pre-existing chronic abnormalities | Persistent ST-segment depression; T-wave inversion; ECG may be normal at rest between episodes | ST-segment elevation myocardial infarction (STEMI) or new left bundle branch block; mirror-image |
| Troponins (ultrasensitive TnI or TnT) | Normal (no myocardial necrosis) | Elevated (NSTEMI) or normal (pure unstable angina without necrosis) | Very high; characteristic rise and fall curve |
| Immediate support | Scheduled medical consultation; resting ECG; cardiovascular assessment; lifestyle modification and optimized medical treatment | Emergency hospital admission without delay; ECG within 10 minutes; troponins at H0 and H1 or H3; anticoagulation; coronary angiography within 24 to 72 hours depending on risk. | Call 9-1-1; emergency cardiac catheterization (primary angioplasty within 90 to 120 minutes); thrombolysis if angioplasty cannot be performed in time |
Cardiovascular risk factors and risk assessment
Angina pectoris is, in the vast majority of cases, the clinical consequence of coronary atherosclerosis, the development of which is favored by modifiable and non-modifiable cardiovascular risk factors. The identification and correction of modifiable risk factors form the cornerstone of primary and secondary prevention of coronary events in Quebec, in line with the recommendations of the Canadian Cardiovascular Society (CCS) and Hypertension Canada.
| Risk factor | Importance and mechanisms | Therapeutic Targets in Quebec |
|---|---|---|
| Dyslipidemia | LDL cholesterol is the main causal factor for coronary atherosclerosis; each reduction of 1 mmol/L in LDL-C reduces the risk of a major cardiovascular event by 20-25%; lipoprotein(a) is a recognized emerging independent risk factor; triglycerides and low HDL-C contribute to residual risk | LDL-C less than 2.0 mmol/L for high-risk primary prevention; less than 1.8 mmol/L for secondary prevention (established coronary artery disease); less than 1.4 mmol/L according to 2019 ESC recommendations for very high-risk patients; statins (atorvastatin, rosuvastatin) as first-line; ezetimibe as second-line; PCSK9 inhibitors (evolocumab, alirocumab) reimbursed by the RAMQ for very high-risk patients or those intolerant to statins |
| Hypertension | High blood pressure increases left ventricular afterload (increased myocardial workload and oxygen demand), accelerates coronary atherosclerosis, and promotes left ventricular hypertrophy; the coronary risk is continuous and log-linear from 115/75 mmHg | Target blood pressure below 130/80 mmHg in patients at high cardiovascular risk and patients with established coronary artery disease according to Hypertension Canada 2023 recommendations; ACE inhibitors or ARBs as first-line treatment in diabetic patients and patients with nephropathy; beta-blockers as first-line treatment in coronary patients with left ventricular dysfunction; thiazides and calcium channel blockers according to clinical profile |
| Type 2 diabetes | Diabetes multiplies the risk of coronary heart disease by 2 to 4; chronic hyperglycemia accelerates atherosclerosis through protein glycation, oxidative stress, endothelial dysfunction, and platelet activation; cardiac autonomic neuropathy promotes silent ischemia; diabetic patients often have diffuse triple-vessel coronary artery disease at the time of diagnosis. | HbA1c less than 7.0% (53 mmol/mol) in general; SGLT2 inhibitors (empagliflozin, canagliflozin, dapagliflozin) and GLP-1 receptor agonists (semaglutide, liraglutide) have demonstrated a reduction in major cardiovascular events regardless of glycemic control in type 2 diabetics at high cardiovascular risk; they are reimbursed by the RAMQ for these indications |
| Smoking | Smoking is the main modifiable cardiovascular risk factor in Quebec; it causes major endothelial dysfunction, promotes coronary spasm, activates platelets, increases blood viscosity and fibrinogen levels, reduces HDL-C, and significantly accelerates the progression of atherosclerosis; the risk is dose-dependent, but even light smoking (less than 5 cigarettes per day) multiplies the risk of heart attack by 2 to 3; the risk decreases rapidly after quitting (50 % in 1 year, returning to non-smoker levels in 5 to 15 years) | Complete smoking cessation; nicotine replacement therapies (patches, gums, lozenges, inhalers; reimbursed by the RAMQ for the first cessation attempt); varenicline (Champix; reimbursed) and bupropion (Zyban) as second-line treatments; behavioral support (J'Arrête helpline 1-866-JARRETE; iCoach application); smoking is a relative contraindication for coronary spasm and multiplies the risk of stent thrombosis. |
| Obesity and sedentary lifestyle | Abdominal obesity (waist circumference > 88 cm in women, > 102 cm in men) is associated with insulin resistance, atherogenic dyslipidemia (small, dense LDL, elevated triglycerides, low HDL), and hypertension; sedentary lifestyle is an independent cardiovascular risk factor; regular physical activity reduces blood pressure, improves lipid profile, reduces HbA1c, and improves coronary functional capacity. | 150 to 300 minutes per week of moderate-intensity aerobic physical activity (brisk walking, swimming, cycling) or 75 to 150 minutes of vigorous-intensity according to Canadian recommendations 2020; cardiac rehabilitation program after any acute coronary syndrome or coronary revascularization (reimbursed by the RAMQ; available in hospitals and certain specialized clinics in Quebec) |
| Family history and age | Family history of premature coronary artery disease in a first-degree relative (before age 55 in father or brother, before age 65 in mother or sister): independent non-modifiable risk factor; heterozygous familial hypercholesterolemia (1/250 to 1/500) is underdiagnosed and should be considered in cases of LDL-C > 5 mmol/L or family history of premature coronary artery disease; cascade screening of relatives is recommended | Systematic screening for familial hypercholesterolemia (Dutch Lipid Clinic Network score, MEDPED criteria); early and aggressive statin treatment starting in adolescence if familial hypercholesterolemia is confirmed; genotyping available in Quebec lipidology centers (CHUM cardiovascular disease prevention center, Montreal Heart Institute) |
Diagnostic investigations
| Review | Information obtained | Indication and limitations |
|---|---|---|
| 12-lead resting ECG | Chronic repolarization abnormalities (inverted T waves, ST depression at rest), sequelae of old myocardial infarction (necrotic Q waves), left bundle branch block, left ventricular hypertrophy, arrhythmias; resting ECG is normal in 50 to 70 % of patients with uncomplicated stable angina | First systematic review in any chest pain assessment; to be performed during the crisis if possible (ischemic ST depression); no value for excluding coronary artery disease if normal at rest |
| Baseline biological assessment | NFS (worsening anemia); creatinine and GFR (renal risk, contraindication to contrast agent); fasting blood glucose and HbA1c (diabetes); complete lipid panel (LDL-C, HDL-C, triglycerides, non-HDL-C, lipoprotein(a) at least once); TSH (worsening hypothyroidism or hyperthyroidism); high-sensitivity troponins (exclusion of ACS if acute presentation) | Systematic in the initial assessment of any suspected coronary heart disease; lipoprotein(a) should be measured at least once in the lifetime of every coronary patient because it is genetically inherited and unaffected by statins (treatments under development: inclisiran, PCSK9, high-dose omega-3). |
| Treadmill or ergometer stress test (standard exercise test) | Detection of exercise-induced ischemia (ST depression greater than 1 mm, horizontal or downsloping, during exercise); maximal functional capacity in METs; heart rate and blood pressure during exercise; symptoms provoked by exercise; criteria for premature termination (ST depression greater than 2 mm, severe anginal pain, hypotension, malignant ventricular arrhythmia) | First-line test for intermediate-probability stable angina with a interpretable resting ECG and adequate exercise capacity; sensitivity of 68 %, specificity of 77 %for obstructive coronary artery disease (poor performance in women); contraindicated in recent ACS < 2 days, resting left bundle branch block, severe aortic stenosis, decompensated heart failure, unstable angina |
| Myocardial perfusion scintigraphy (technetium or thallium SPECT) with pharmacological stress (adenosine, dipyridamole, regadenoson) | Quantification of regional myocardial perfusion at rest and during exercise or after pharmacological stress; detection and localization of ischemic territories; assessment of left ventricular ejection fraction; assessment of myocardial viability | Sensitivity of 87 %, specificity of 73 %for obstructive coronary artery disease; indicated if baseline ECG is uninterpretable (left bundle branch block, pacemaker, pre-excitation) or if the patient cannot perform sufficient effort; available in nuclear imaging centers of university hospitals and some Quebec regional hospitals; reimbursed by the RAMQ with justified medical indication |
| Stress echocardiogram (dobutamine or exercise) | Detection of ischemia-induced left ventricular segmental kinetic anomalies; assessment of systolic and diastolic function; associated valvulopathies; sensitivity and specificity of 80 to 85 % | Alternative to scintigraphy if radiation is to be minimized (especially for young women); particularly useful for patients with left bundle branch block at rest (falsely positive septal scintigraphy), for assessing myocardial viability, and for investigating microvascular ischemia (stress echocardiography with coronary Doppler flow) |
| Coroscanner (coronary computed tomography angiography, CCTA) | Non-invasive visualization of epicardial coronary artery anatomy; detection and quantification of atherosclerotic stenosis; coronary artery calcium (CAC) score as a marker of global atherosclerotic burden; FFR-CT (fractional flow reserve calculation by computational fluid dynamics) for hemodynamic assessment of intermediate stenosis | High sensitivity (>95 %) and excellent negative predictive value for excluding obstructive coronary artery disease; recommended as first-line in the 2019 ESC guidelines for patients with low-to-intermediate pre-test probability; avoids invasive coronary angiography in 50-60 % of cases; limitations: poor quality with irregular rhythm (AF) or significant coronary calcifications (CAC score > 400); available in major Quebec imaging centers; reimbursed by the RAMQ upon cardiological indication |
| Coronary angiography (left heart catheterization) | Direct visualization of coronary anatomy and angiographic quantification of stenoses; measurement of fractional flow reserve (FFR) or instantaneous wave-free ratio (iFR) for functional assessment of intermediate stenoses; left ventriculography (EF, regional wall motion); left diastolic ventricular pressure | Gold standard examination; allows for percutaneous revascularization (percutaneous transluminal coronary angioplasty, PTCA, with drug-eluting stent placement) during the same catheterization; indicated if non-invasive tests are positive or highly suggestive, angina refractory to optimized medical treatment, patients with very high pre-test probability or high risk, preparation for valvular or other cardiac surgery; very rare serious complication in expert centers (less than 0.1 %: coronary dissection, stroke, peri-procedural infarction) |
Medical treatment of stable angina
The therapeutic management of stable angina pectoris is based on two complementary and non-substitutable objectives: relieving anginal symptoms and improving quality of life on one hand, and reducing the risk of major cardiovascular events (myocardial infarction, cardiovascular death) on the other. These two objectives are not always achieved by the same treatments, and their prioritization guides individualized therapeutic decisions.
| Treatment | Mechanism and benefits | Practical arrangements in Quebec |
|---|---|---|
| Sublingual nitroglycerin (trinitrin) | Direct venous and coronary vasodilation through nitric oxide (NO) release; reduction of left ventricular preload and afterload; angina attack relief in 1 to 3 minutes; duration of action 15 to 30 minutes | 0.3 mg or 0.6 mg sublingual tablets (Nitrostat; reimbursed by the RAMQ); sublingual spray (Nitrolingual; reimbursed by the RAMQ); to be placed under the tongue or sprayed; sitting or lying down to prevent orthostatic hypotension; repeat every 5 minutes up to 3 times if pain persists; call 9-1-1 if no relief after 3 doses; store away from light and heat; renew the bottle every year (gradual loss of effectiveness) |
| Beta-blockers | Reduction in heart rate, contractility, and blood pressure (reduction in myocardial oxygen consumption); increased diastolic perfusion time (coronary perfusion occurs mainly during diastole); first-line anti-anginal and cardioprotective agent in cases of post-infarction left ventricular dysfunction or heart failure with reduced ejection fraction. | Metoprolol succinate (Toprol-XL, Betaloc ZOK; reimbursed by RAMQ); bisoprolol (Monocor; reimbursed); carvedilol (Coreg; reimbursed if LV dysfunction); atenolol (less recommended as first-line, less favorable pharmacokinetics); target: resting heart rate of 55 to 65 beats per minute; contraindicated in severe asthma, high-grade AV block, severe bradycardia; do not stop abruptly (anginal rebound) |
| Calcium channel blockers | Coronary and peripheral vasodilation; reduction of afterload; dihydropyridines (amlodipine, felodipine, nifedipine LP) act primarily on vasodilation without significant negative chronotropic effect; non-dihydropyridines (verapamil, diltiazem) also reduce heart rate and contractility; particularly effective in vasospastic angina (Prinzmetal) and microvascular angina | Amlodipine (Norvasc; RAMQ covered): 5 to 10 mg once daily; diltiazem extended-release (Cardizem CD, Tiazac; covered): 120 to 360 mg once daily; verapamil ER (Isoptin SR; covered): 120 to 480 mg daily; non-dihydropyridines are contraindicated in combination with beta-blockers (risk of AV block and bradycardia) and in case of severe systolic LV dysfunction (EF less than 35 to 40 %) |
| Long-acting nitrates | Sustained venous and coronary vasodilation; reduction of preload and myocardial workload; prevention of angina attacks; reduced efficacy due to tolerance (tachyphylaxis) if administered continuously without a free period of at least 8 to 10 hours per 24 hours | Isosorbide mononitrate (Imdur; RAMQ covered): 30 to 120 mg in the morning; transdermal nitroglycerin patch 0.2 to 0.6 mg/hour (Minitran, Nitro-Dur; covered): apply in the morning and remove after 12 to 14 hours (mandatory nighttime free period to avoid tolerance); contraindicated with PDE5 inhibitors (sildenafil, tadalafil, vardenafil) due to the risk of potentially fatal severe hypotension |
| Ivabradine (Lancora) | Inhibition of the sinus node If current (pure bradycardia without inotropic or vascular effect); reduction of heart rate at rest and during exercise; reduction of myocardial oxygen consumption; indicated as a second-line treatment if beta-blockers are insufficient or poorly tolerated in patients with sinus rhythm | Reimbursed by RAMQ in coronary patients with heart rate above 70 bpm in sinus rhythm despite optimized beta-blocker, or in case of contraindication to beta-blockers; dosage 5 to 7.5 mg twice daily; contraindicated in atrial fibrillation (lack of effect), in combination with strong CYP3A4 inhibitors (azole antifungals, macrolides, HIV protease inhibitors) |
| Ranolazine (Ranexa) | Late sodium current inhibitor (INaL), reducing intracellular calcium overload of the ischemic myocyte without affecting heart rate or blood pressure; purely metabolic anti-anginal; effective in combination with standard anti-anginal treatments | Available in Canada; limited RAMQ coverage at time of writing; dosage 500 to 1,000 mg twice daily; prolongs QTc (ECG monitoring); significant drug interactions (CYP3A4 inhibitors); may be used in patients where bradycardia or hypotension limit optimization of other treatments |
| Low-dose aspirin (antiplatelet) | Irreversible inhibition of platelet cyclooxygenase-1 (COX-1); reduction of thromboxane A2 synthesis (vasoconstrictor and aggregating agent); reduction of the risk of myocardial infarction and cardiovascular death in patients with established coronary artery disease (secondary prevention). | Aspirin 80 to 100 mg once daily (covered by RAMQ); in coronary patients with established coronary artery disease, aspirin is a lifelong treatment unless contraindicated (true allergy, active gastrointestinal bleeding); in patients on dual antiplatelet therapy after angioplasty (aspirin + clopidogrel, ticagrelor, or prasugrel), the duration of dual antiplatelet therapy is guided by the type of stent, the clinical context, and the bleeding risk jointly assessed by the cardiologist. |
| Statins | Reduction of LDL-C (main driver of atherosclerosis); stabilization of atherosclerotic plaques (pleiotropic effects on inflammation, vascular endothelium, and thrombosis); 25-35% reduction % in the risk of major cardiovascular events per mmol/L of LDL-C reduction in secondary prevention | Atorvastatin 40 to 80 mg (Lipitor; RAMQ-reimbursed) or rosuvastatin 20 to 40 mg (Crestor; reimbursed) as first-line treatment in any coronary patient, regardless of baseline LDL-C; lifelong treatment; monitor transaminases once after initiation; CPK if significant myalgias; no systematic transaminase monitoring recommended by the CCS after stabilization |
| IEC or ARB-II | Inhibition of the renin-angiotensin-aldosterone system; reduction of blood pressure and afterload; cardioprotection independent of the antihypertensive effect in high-risk coronary patients (ramipril in the HOPE trial, perindopril in the EUROPA trial); nephroprotection in diabetics | Ramipril (Altace; RAMQ reimbursed) or perindopril (Coversyl; reimbursed) in all coronary patients with LV dysfunction, diabetes, or hypertension; telmisartan (ARB) if dry cough with ACE inhibitors (frequent: 5 to 20 % of patients, especially Asians); monitor potassium and creatinine 2 weeks after initiation, then annually |
Coronary revascularization: angioplasty and surgery
Myocardial revascularization, by percutaneous transluminal coronary angioplasty (PTCA) with implantation of a new generation drug-eluting stent or by surgical coronary artery bypass grafting (CABG), is indicated in cases of stable angina refractory to optimized medical treatment, anatomically and functionally significant coronary lesions, or high-risk coronary artery disease (left main coronary artery disease, three-vessel disease with left ventricular dysfunction). The decision to revascularize should consider coronary anatomy (SYNTAX score), left ventricular function, comorbidities, and the patient's informed preferences, and should be made in a multidisciplinary Heart Team discussion involving an interventional cardiologist and a cardiac surgeon.
The ISCHEMIA study (2020), whose results have modified contemporary cardiological practice, demonstrated that in patients with stable angina and moderate to severe myocardial ischemia detected by functional imaging, an early invasive revascularization strategy (angioplasty or bypass surgery) does not provide superior benefit in terms of mortality and myocardial infarction compared to optimized medical treatment alone over a median follow-up period of 3 to 7 years. However, revascularization remains superior for the control of anginal symptoms and improvement of quality of life in symptomatic patients. These results confirm the crucial importance of optimized medical treatment as a universal therapeutic foundation, with revascularization being reserved for patients whose symptoms persist despite this treatment or who present with anatomically very high-risk lesions.
Consult at Clinique Omicron
Clinique Omicron's physicians, at our Quebec locations, are able to assess all non-emergency angina-like chest pain, perform a resting ECG and complete cardiovascular workup (lipids, blood glucose, HbA1c, CBC, creatinine, TSH), and refer to a cardiologist within the appropriate timeframe according to CCS classification and pre-test probability of coronary disease. Our clinicians also monitor known stable coronary patients: renewing and adjusting anti-anginal and cardioprotective treatments, monitoring statin and aspirin compliance, controlling modifiable risk factors (blood pressure, LDL-C, HbA1c, smoking), updating vaccinations (annual flu, COVID-19, pneumococcus in high-risk patients), and providing support for cardiac rehabilitation. Teleconsultation is available for monitoring stable patients and managing intercurrent symptoms. Any new chest pain at rest, any change in the usual anginal pattern, or any episode of pain that does not respond to nitroglycerin, requires an immediate call to 9-1-1 and evaluation by the hospital emergency department. Make an appointment at one of our branches in Quebec.
The content of this page is provided for informational purposes only and is not intended to replace the advice of a qualified healthcare professional. Consult a physician for any symptoms, questions or decisions you may have regarding your health.
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