Ischemic Heart Disease PDF

CANLAS, HAPITAN, MOSTAZA, RAMOS, SUBIJANO, SUGATAN, TEJARES | EBPT 1 1 ISCHEMIC HEART DISEASE also known as coronary artery disease (CAD) Characterized by an imbalance between myocardial oxygen supply and demand This is due to the red...

CANLAS, HAPITAN, MOSTAZA, RAMOS, SUBIJANO, SUGATAN, TEJARES | EBPT 1 1 ISCHEMIC HEART DISEASE also known as coronary artery disease (CAD) Characterized by an imbalance between myocardial oxygen supply and demand This is due to the reduction of blood flow to the heart muscle, because of atherosclerotic plaque buildup in the coronary arteries may present as Acute Coronary Syndrome which includes unstable angina, NSTEMI, STEMI it can also present as Stable Ischemic Heart Disease which manifest as either chronic stable exertional angina or ischemia without clinical symptoms (silent ischemia) EPIDEMIOLOGY Most common, serious, chronic, life-threatening illness in the United States and in the Philippines. DETERMINANTS OF MYOCARDIAL OXYGEN DEMAND Ischemic Heart disease is one of the top 3 causes of death The major determinants of MVO2 includes: in the Philippines from January to August 2023 (Philippine 1. Heart Rate Statistic Authority (2023) 2. Myocardial Contractility PATHOPHYSIOLOGY 3. Intramyocardial Wall Tension The primary cause of Ischemic Heart Disease is the fixed HEART RATE decrease in supply caused by the long-standing, well- developed atherosclerosis plaque it is a slow, progressive increasing heart rate increases the oxygen demand. process where plaques composed of lipids, inflammatory As the heart beats faster, the myocardial cells consume cells and fibrous elements build up in the walls of coronary more energy in order to maintain the contraction and arteries relaxation process, increasing oxygen demand. these plaques limit the flow of oxygen-rich blood to the MYOCARDIAL CONTRACTILITY heart leading to ischemia this refers to the heart muscle’s ability to contract with risk factors for plaque formation includes: force. o Smoking When contractility increases, the heart pumps more o Dyslipidemia forcefully, ejecting more blood each beat. o Hypertension o Enhanced force of contractility requires more energy o Diabetes mellitus since oxygen is essential for ATP production the o Genetics demand for oxygen also increase in response to the An imbalance between the oxygen supply and demand increased energy need. leads to myocardial ischemia. Myocardial ischemia leads to angina pectoris. INTRAMYOCARDIAL WALL TENSION o angina pectoris - chest pain behind the sternum, which, in the sense of is the most significant determinant of myocardial oxygen the term, means a “strangling feeling in the chest”. demand. Angina is most often the result from an imbalance in increased MVO2 is directly related to the radius or size of myocardial oxygen supply and demand (MVO2). the ventricular cavity and blood pressure (BP), and The pathophysiology of Stable IHD is driven by an increase indirectly related to the ventricular muscle mass. in the myocardial oxygen demand (MVO2) in the setting of o increased myocardial oxygen demand is directly related to the radius or size of the ventricular cavity and blood pressure (BP), and indirectly a fixed decrease in myocardial oxygen supply. The related to the ventricular muscle mass. As the radius of the ventricular etiology of the fixed decrease in supply is long standing, cavity increases, the wall tension increases. Higher wall tension means well developed atheroscerotic plaque. the myocardium needs to worker harder to pump blood, which directly Unlike Acute Coronary Syndrome (ACS), where plaque rupture leads to increases oxygen demand. sudden thrombus formation and decreased blood flow, the plaque in SIHD o another determinant of wall tension is blood pressure. As blood pressure are stable with a reduced lipid core and firm calcified outer layer. increases, the force that the ventricular muscle needs to generate to push blood into the circulation also rises. this increased workload thus, the heart requires more oxygen to sustain its contraction, thus increasing myocardial oxygen demand. o lastly, ventricular muscle mass. thickening of ventricular wall or ventricular hypertrophy occurs as a result of prolonged hypertension. And increased wall thickness reduces wall tension however, it also increases the muscle mass. larger muscle mass means more myocardial cells to supply with oxygen, thereby indirectly increasing myocardial oxygen demand. NOREPINEPHRINE The release of Norepinephrine by adrenergic nerve endings in the heart and blood vessels triggered by physical exertion, emotion or mental stress.  CANLAS, HAPITAN, MOSTAZA, RAMOS, SUBIJANO, SUGATAN, TEJARES | EBPT 1 2 § Nitric Oxide OTHER FACTORS § Prostacyclin Rapid physical activity and movements like raising the arms § Bradykinin can also lead to chest pain. § this can increase coronary blood flow 4 to 5 fold over normal o The speed at which oxygen demand increases—linked to how quickly a resting condition. task is performed. o mental and emotional stress can provoke angina by heightening The increase in coronary flow above resting condition is norepinephrine levels and lowering vagal activity. called coronary flow reserve. Other factors, such as cold exposure and low blood sugar, Atherosclerotic plaque forms in the large epicardial vessels can also contribute to an increased heart rate and potential (R1). As plaque grow, resistance in the R1 vessels increases. angina. o as stated before, in normal and healthy conditions R1 offers limited resistance to flow. However, as atherosclerosis progress,resistance in the R1 vessels increases. through autoregulation the increase in DETERMINANT OF MYOCARDIAL SUPPLY resistance from the R1 is offset by vasodilation inthe R2 to maintain The amount of oxygen delivered to the heart muscle. The flow. primary determinants includes: Plaque that occupy less than 50% to 70% of the vessel’s 1. Coronary Blood Flow luminal diameter are often referred to as “nonobstructive” 2. Heart Rate and Systole and rarely produce ischemia or angina 3. Oxygen Extraction and Oxygen Carrying Capacity o but are prone to rupture, which can lead to ACS. 4. Coronary Collateral Circulation Plaque that occupy 70% or more of the luminal diameter 5. Coronary Vasospasm and Prinzmetal’s angina are considered “obstructive” o and the R2 vessels must fully dilate to maintain normal coronary flow. At this stage, coronary flow reserve is nearly exhausted, and even CORONARY BLOOD FLOW minimal physical exertion can lead to myocardial ischemia and angina. The amount of exertion a patient can endure is largely based on the extent of vessel stenosis and the remaining coronary flow reserve. When narrowing of the luminal diameter exceeds 90% it is called critical stenosis. The endocardial flow reserve is exhausted Nonobstructive: Occupies 50-70%: Obstructive: Occupies 70% or more: Critical stenosis: Occupies 90% Meeting the metabolic demands of the myocardium is centered on the ability to maintain adequate coronary HEART RATE AND SYSTOLE blood flow and coronary arterial pressure. In normal conditions, coronary blood flow ranges from 0.7 to 1.0 mL/min/g of myocardium. The coronary vasculature consists of: coronary vasculature refers to the blood vessels that is responsible for transporting oxygen rich blood to the myocardium and remove deoxygenated blood o Large epicardial vessels (R1) § Conductance Vessels § Conduits for blood flow § the large epicardial vessel which is also called as conductance vessels. R1 serves as conduits or pathway for blood flow. It usually When heart rate increases, the myocardium requires more offer minimal resistance under normal conditions. oxygen but also reduces myocardial oxygen supply o Smaller endocardial vessels (R2) Most tissue and organ perfused during systole § Resistance Vessels The heart is the only organ that is perfused during diastole, § Regulate flow based on MVO2 the phase of myocardial relaxation. § the smaller endocardial vessel also called as resistance vessels regulates flow by constricting or dilating based on the myocardial There are two physiological explanations: oxygen demand 1. The pressure created in the ventricles during systole The total resistance to coronary blood flow is the sum of creates an increase in pressure in the coronary resistance in the R1 and R2 vessels. circulation well above the pressure for coronary When the heart is at rest, MVO2 is low, the R2 vessels perfusion (50- 60 mm Hg). Only during diastole do the constricts pressures drop sufficiently to allow coronary flow. o because the need for blood flow is reduced. 2. During a typical cardiac cycle, the myocardium spends During exercise or stress, MVO2 increases, the R2 vessels twice as much time in diastole compared to systole. This dilate. reduces the time for myocardial perfusion, and thus o this is to provide more blood flow to the heart. oxygen supply is significantly diminished. The process of constricting and dilating the resistance vessels based on MVO2 is called autoregulation. In response to increased in MVO2, several vasodilators are released to increase coronary blood flow. o Vasodilators:  CANLAS, HAPITAN, MOSTAZA, RAMOS, SUBIJANO, SUGATAN, TEJARES | EBPT 1 3 OXYGEN EXTRACTION AND OXYGEN CARRYING CORONARY VASOSPASM AND PRINZMETAL’S ANGINA CAPACITY In most patient with SIHD, have an obstructive coronary Two additional determinants of myocardial oxygen supply stenosis and exertion induced ischemia. Since the size of the are: obstructive lesion does not change acutely, the amount of 1. Myocardial oxygen extraction exertion needed to induce angina is often predictable in an § refers to the amount of oxygen removed from the individual patient. blood. Some patients have variable threshold angina. In these § Increase oxygen extraction from the arterial blood patients, the amount of exertion needed to provoke chest 2. Oxygen-carrying capacity pain differs from day to day. § Arterial oxygen content is related to hemoglobin The variability occurs due to fixed obstruction of concentration and oxygen saturation. atherosclerosis and transient vasospasm. § Patients with Anemia (low hemoglobin) or hypoxia Some patients have variant angina, also known as (low oxygen saturation) have lower than normal Prinzmetal's angina oxygen-carrying capacity. Patients with variant angina usually do not have flow- § high hemoglobin concentration increase the blood’s oxygen- carrying capacity. obstructing atherosclerotic plaques in their coronary § Patients with SIHD often require transfusion when arteries, but instead, have vasospasm in epicardial vessels. hemoglobin concentration fall below 9-10 g/dL o The vasospasm is due to reduced production of under normal condition, the coronary blood’s ability to carry oxygen is vasodilators and an exaggerated response to relatively fixed. this means that when the heart’s oxygen demand increase endogenous vasoconstrictors example during physical activity the compensatory mechanism is to extract more oxygen from the blood that is already delivered. typically the heart Patients with Prinzmetal’s Angina are often younger than extracts 75% of the available oxygen from arterial blood this means that patients with SIHD. the myocardium is already using most of the oxygen delivered to it, leaving o Characterized as Chest pain at rest, often in the early little room for increased extraction during high oxygen demand. morning, and have transient ST segment elevation on the ECG. CORONARY COLLATERAL CIRCULATION Vasospasm-induced angina is often more common in the When a coronary stenosis exceeds 70%, endocardial morning, likely due to the circadian release of vessel pressure falls due to maximized autoregulation. This vasoconstrictors, which naturally occurs at higher levels contributes to the severity and duration of the episodes of early in the day. exertion-induced ischemia. Other triggers include exposure to cold temperatures, In patients with SIHD, pre-existing collateral vessels emotional stress, and mental stress, which can all lower the develop in a process termed arteriogenesis. angina threshold by increasing the likelihood of vasospasm. o Narrowed arteries lead to ischemic episodes. This trigger angina. OTHER FACTORS o In response to ischemic episode, the body stimulate While atherosclerotic coronary stenosis is the leading cause nitric oxide synthase and lead to production of vascular in the development of SIHD and angina, there are endothelial growth factor and basic fibroblast growth additional pathophysiologic mechanisms that also contribute factor. to disease onset and progression. These mechanisms o The combination of altered coronary pressure, growth include: factors, and endogenous vasodilators (NO, o Endothelial dysfunction prostacyclin) changes native collateral vessels of § due to reduced NO synthesis which may lead to ischemia. approximately 200 μm into mature vessels that can o Microvascular dysfunction reach 1-2 mm in diameter. § vessels don’t dilate as they should in response to the increase need of the heart like exercise leading to inadequate blood flow. While most functional collateral flow develops from the process of angiogenesis, collateral perfusion can also occur o Vasospasm from the development of new collateral vessels in a process o Platelet activation and coagulation § thrombus formation that can block the artery called angiogenesis. o Inflammation o This is driven by physical forces and growth factors but produces smaller, capillary-like vessels. PHENOTYPES OF ISCHEMIC HEART DISEASE New collateral vessels may develop: ACUTE CORONARY SYNDROME (ACS) o in the border between ischemic and nonischemic regions of the myocardium. UNSTABLE ANGINA o within the ischemic region, reducing the distance blood clots that block an artery partially or totally between capillaries and improving oxygen delivery to because your heart doesn’t get enough blood flow and affected heart tissues. oxygen Coronary collateral circulation plays a crucial compensatory role in ischemic heart disease by providing alternative blood flow pathways to areas of the heart where Attacks are more unpredictable and can continue despite normal coronary arteries are narrowed or blocked. The two processes, resting. arteriogenesis and angiogenesis, help limit the severity of ischemia, but their effectiveness varies. This adaptive mechanism can sometimes alleviate symptoms and reduce the risk of major cardiovascular events in patients with severe coronary NON-ST SEGMENT ELEVATION MYOCARDIAL INFARCTION artery disease. (NSTEMI) indicates partial blockage of one of the coronary arteries Anrteriogenesis: Pre-excisting collateral vessels causing reduced blood flow of oxygen-rich blood to the Angiogenesis: New collateral vessels heart muscles  CANLAS, HAPITAN, MOSTAZA, RAMOS, SUBIJANO, SUGATAN, TEJARES | EBPT 1 4 ST SEGMENT ELEVATION MYOCARDIAL INFARCTION Once a patient has entered the symptomatic phase, the patient may exhibit a (STEMI) stable or progressive course, revert to the asymptomatic stage, or die suddenly Indicates a total blockage of the involved coronary artery Asymptomatic or Silent Ischemic heart disease can only diagnosed when a and that the heart muscle is currently dying. proper diagnosis is made through proper screening. o is characterized as asymptomatic, or silent, when it occurs in the absence of angina or an anginal equivalent. STABLE ISCHEMIC HEART DISEASE (SIHD) o When present, asymptomatic ischemia is correlated positively with incident ischemic heart disease and confers an unfavorable prognosis CHRONIC STABLE ANGINA (Maron et al,. 2017). o is frequently observed among patients with diabetes, presumably due a type of chest pain that happens when your heart muscle to the associated neuropathy. needs more oxygen than usual but it’s not getting at that o Other patient populations at risk for asymptomatic ischemia include those with a previous MI. moment because of heart disease. It can happen when it’s Ischemia is detected in nearly twice as many asymptomatic patients with cold outside or when exercising. diabetes compared to age and gender-matched patients without diabetes when myocardial perfusion imaging is added to conventional exercise ISCHEMIA WITHOUT CLINICAL SYMPTOMS electrocardiogram (ECG) testing. occurs when the heart temporarily doesn't receive enough RISK FACTORS blood and oxygen but the person with oxygen deprivation RISK FACTORS OF ATHEROSCLEROSIS doesn’t notice any symptoms or effects Effect of risk factors is multiplicative rather than additive It is important to distinguish between relative risk and SIGNS AND SYMPTOMS absolute risk CARDINAL SYMPTOM IN PX WITH SIHD: Chest pain (angina) from exertion ABSOLUTE RISK The major symptom of chronic ischemic heart disease is AGE AND SEX angina pectoris, with a clinical diagnosis based on five Premenopausal women have lower rates of disease than features: (Crawford, 2017) men o the pain is a deep visceral pressure or squeezing This sex difference disappears after the menopause sensation, rather than sharp, stabbing, or pinprick-like pain. POSITIVE FAMILY HISTORY o pain almost always has some substernal component, Runs in families although some patients complain of pain only on the due to a combination of shared genetic, environmental, and right or left side of the chest, upper back, or lifestyle factors epigastrium. RELATIVE RISK o pain may radiate from the thorax to the jaw, neck, or arm. SMOKING o When angina is usually precipitated by exertion, Consistent use emotional upset, or other events that obviously increase HYPERTENSION myocardial oxygen demand, such as rapid Directly proportional tachyarrhythmias or extreme elevations in blood pressure. HYPERCHOLESTEROLAEMIA o When angina pectoris is transient and lasts between 2 Directly proportional to serum cholesterol concentrations and 30 minutes. (LDL) § Chest pain that lasts longer than 30 minutes is more consistent with myocardial infarction; pain lasting less than 2 minutes is DIABETES MELLITUS unlikely to be due to myocardial ischemia. potent risk factor for all forms of atherosclerosis SYMPTOMATIC ASYMPTOMATIC o Men with type 2 diabetes: 2-4 fold greater annual risk more common “Silent IHD” of CAD o Women with type 2 diabetes: 3-5 fold risk characterized by chest characterized as asymptomatic, or discomfort due to either angina silent, when it occurs in the absence HAEMOSTATIC FACTORS pectoris or acute myocardial of angina or an anginal equivalent. Platelet activation and high levels of fibrinogen infarction patient may exhibit a stable or When present, asymptomatic Antiphospholipid antibodies - recurrent arterial progressive course, revert to the ischemia is correlated positively thrombosis asymptomatic stage, or die with incident ischemic heart disease PHYSICAL ACTIVITY suddenly and confers an unfavorable prognosis (Maron et al,. 2017). Physical inactivity roughly doubles the risk of Coronary Heart Disease frequently observed among patients with diabetes, presumably OBESITY due to the associated neuropathy. Often associated with HTN and cardiovascular disease Other patient populations at risk for asymptomatic ischemia include ALCOHOL those with a previous MI. Excess consumption Symptomatic patients are more common, and the symptomatic phase is characterized by chest discomfort due to either angina pectoris or acute OTHER DIETARY FACTORS myocardial infarction. Diets deficient in fresh fruits, vegetables and polyunsaturated fatty acids (PUFA)  CANLAS, HAPITAN, MOSTAZA, RAMOS, SUBIJANO, SUGATAN, TEJARES | EBPT 1 5 PERSONALITY DIAGNOSTIC AND PROGNOSIS Although there is little or no evidence to support the popular 12-LEAD ECG belief that stress is a major cause of CAD cornerstone of diagnostic testing in suspected IHD patients. As an overview, ECG records the electrical activity of the heart through the SOCIAL DEPRIVATION skin via electrodes and displays it graphically. The graph shows the hearts overall electrical potential or voltage as it changes over time during a cardiac cycle. The 12-leads of the ECG represent the 12 electrical views CLINICAL PRESENTATION ASSESSMENT OF SYMPTOMS of the heart from 12 different angles. PQRST APPROACH So for patients with suspected IHD, a resting ECG is Since pain is subjective, most often than not, clinicians rely recommended and should be recorded during the initial on the patient’s self-report on their own pain. check-up Therefore, healthcare providers use the PQRST approach to In the resting state, the ECG normal in ≥50% of patients accurately describe, assess and document a patient’s pain with SIHD The method also aids in the selection of appropriate pain In SIHD patients with a normal ECG at rest, about 50% medication and evaluating the response to treatment. will develop ischemic ST-T wave changes during an For us pharmacists, this method could be useful to gather episode of angina information that we can use in counselling our patients and also assist the physician in making their recommendations. FACTOR PRESENTATION IN STABLE ISCHEMIC HEART DISEASE Precipitating Typically brought on by some level of exercise factors or exertion Palliative Relieved by rest w/ or w.o a sublingual measures nitroglycerin in 5-10 minutes Quality of the pain Continuous squeezing, heaviness, or tightness Region Substernal Radiation Left or right arm, back, down into the abdomen, up into the neck Severity Left or right arm, back, down into the abdomen, up into the neck Temporal Pattern Pain lasts less than 20 minutes and is usually (timing) relieved in 5-10 minutes CAD-CORONARY ANGIOGRAPHY P = PRECIPITATING FACTORS Most HCPs ask questions like, What were you doing when the pain started? Defines coronary anatomy, including the location, length, What seems to trigger it? and typically, pain brought about by IHD is due to diameter, and contour of the epicardial coronary arteries some level of exercise and exertion o the presence and severity obstruction (arrows pointing P = PALLIATIVE MEASURES to obstruction) We ask, What relieves your pain? IHD patient’s chest pain is relieved by rest o the nature of the obstruction even with or without SL nitroglycerin in 5-10 minutes o and coronary blood flow. Q = QUALITY Here we ask the patient to describe their pain. Is it crushing? Para po bang Invasive coronary angiography that currently remains the may nakaupo na elepante sa dibdib? Is it sharp? May kirot po ba? Those gold standard and requires arterial access, usually to the type of questions femoral artery. This test has two goals: R = REGION AND RADIATION o to assess a patient’s risk of death future cardiovascular Questions like where did the pain start? Does it radiate? Umaabot ba sa events through characterization of the presence and kamay? Most often, chest pain starts at the substernal region and can radiate extent of obstructive CAD; to the arms, back, abdomen and neck. S = SEVERITY o to ascertain the feasibility of percutaneous or surgical We ask our patient to rate their pain through a visual analog scale. While revascularization. pain is subjective, those who have chest pain report a 5 or higher on 10 point § Useful in determining the fractional flow reserve (FFR) in patients scale with obstructive coronary stenosis. § an invasive technique that requires arterial access. T = TEMPORAL PATTERN OR TIMING So we ask questions like when/what time did the pain start, how long did it last? How often? Most of the time, stable IHD patients experience pain that lasts less than 20 minutes and is usually fully relieved in 5-10 minutes. CHARACTERISTIC OF CARDIAC AND NON-CARDIAC PAIN SYMPTOMATIC ASYMPTOMATIC Description of Heavy, tight, pressure, Sharp, stabbing, Pain dull, band, squeezing shooting, needle Site Central anterior Left sub mammary Left arm, right arm, Right sub mammary teeth Interscapular, epigastric Precipitants Exercise, emotion, cold, Stress, posture, post prandial particular movements of arms or neck, swallowing (odynophagia)  CANLAS, HAPITAN, MOSTAZA, RAMOS, SUBIJANO, SUGATAN, TEJARES | EBPT 1 6 EXERCISE STRESS TESTING o and reduce both symptomatic and silent episodes of myocardial ischemia. Is also a type of test using ECG but now we ask the patient to do some exercise or the myocardium can also be MOA: Beta blockers reduce myocardial oxygen stressed pharmacologically with adenosine, consumption by reducing heart rate, myocardial dipyridamole, or dobutamine. contractility and afterload, with attenuation of cardiovascular remodeling by decreasing LV wall tension It is a relatively easy and inexpensive method for with long term use detecting CAD and can provide important diagnostic and o ↓HR ↓CO ↓BP prognostic information, especially when conducted with a nuclear imaging study to evaluate myocardial perfusion. o ↓ Myocardial Oxygen Demand Reductions in heart rate may also improve myocardial oxygen delivery by prolonging diastole filling time and increasing myocardial perfusion. Recommended to initiate a beta blocker by oral route for all patients o within the first 24 hours unless contraindications are present. o Use of IV beta blockers should be considered with caution. o If β-blocker therapy needs to be discontinued, doses need to be tapered over 2 to 3 weeks to prevent abrupt withdrawal. CALCIUM CHANNEL BLOCKERS Non-DHP CCBs: verapamil and diltiazem and DHP CCBs nifedipine, amlodipine and felodipine Effectively reduce the frequency and duration of angina episodes in patients with SIHD. MANAGEMENT TREATMENT GOALS Reduce myocardial volume oxygen, as well as provide some increase in supply by inducing coronary vasodilation Complete (or nearly complete) elimination of angina chest and preventing vasospasm. pain and return to normal activities MOA: Long Term Goals o DHP: block L-type calcium channels primarily in the o Slow progression of atherosclerosis vascular smooth muscle with minimal effect on the o Prevent complications such as myocardial infarction myocardium leading to reduced oxygen demand (MI), heart failure, stroke and death o Non-DHP: block L-type calcium channels mostly in the Therapeutic Goals myocardium with minimal effect on the vascular o Prolong life smooth muscle leading to reduced oxygen demand o Reduce symptoms of angina o Improve quality of life (QoL) It may be recommended to use oral long acting calcium antagonists for recurrent ischemia in the absence of PHARMACOLOGIC TREATMENT contraindication and when beta blockers and nitrates are ACC/AHA CLASS OF RECOMMENDATIONS FOR maximally used. PHARMACOTHERAPY TO RELIEVE SYMPTOMS Common side effects of CCBs vary between the two classes. Class I Class IIa o Patients taking non-DHP CCBs may experience Initial therapy for relief of Initial therapy (instead of 𝜷- bradycardia, hypotension, atrioventricular block, and symptoms: 𝜷-blockers (LOE B) blockers) for relief of symptoms: symptoms of LV depression. Long acting nondihydropyridine o Non-DHP CCBs should not be used in patients who calcium channel blocker have contraindications or cannot tolerate β-blockers (verapamil or diltiazem) (LOE B) due to these same effects. When 𝜷-blockers is Substitute for 𝜷-blockers when it is contraindicated or with side contraindicated or with side effects: NITRATES effects: Calcium channel blockers Ranolazine (LOE B) Organic nitrates were found to have antianginal properties or long acting nitrates (LOE B) over one hundred years ago when Murrell first reported in If 𝜷-blocker treatment is If 𝜷-blockers treatment is 1879 the ability of a 1% nitroglycerin solution administered unsuccessful: add with Calcium unsuccessful for initial treatment: orally to relieve and prevent angina attacks. channel blocker + Long acting add Ranolazine in combination nitrates (LOE B) with 𝜷-blockers (LOE A) Organic nitrates are prodrugs that require Immediate relief of angina: biotransformation into the active compounds. Sublingual nitroglycerin or o This process leads to denitration of the nitrate and the nitroglycerine spray (LOE B) release of nitric oxide, also known as EDRF (endothelium-derived relaxing factor) PHARMACOLOGIC THERAPY TO RELIEVE SYMPTOMS MOA: Release NO in smooth muscle à activates guanylyl RECOMMENDATIONS cyclase and increase cGMP à vasodilation and increase BETA-BLOCKERS blood flow Propranolol, atenolol and metoprolol It is recommended that nitrates (sublingual tablet or spray), followed by intravenous (IV) administration, be Commonly used in the management of patients with Stable administered for the immediate relief of ischemic and Ischemic Heart Disease associated symptoms.  CANLAS, HAPITAN, MOSTAZA, RAMOS, SUBIJANO, SUGATAN, TEJARES | EBPT 1 7 It is NOT recommended to administer nitroglycerine (NTG) increases myocardial oxygen supply in vessels with critical or other nitrates within 24 hours of sildenafil use or within stenosis. 48 hours of tadalafil use. PERCUTANEOUS CORONARY INTERVENTIONS Common side effects from nitrate therapy include Use of balloon angioplasty with stent placement as well as headache, flushing, nausea, postural hypotension, and other less commonly performed intracoronary procedures syncope. such as rotational atherectomy and aspiration thrombectomy. RANOLAZINE A catheter is guided into the coronary blood vessels through Unlike other agents used for angina either the femoral or radial arterial. ranolazine does not impact HR, BP, the inotropic state, or The deflated balloon is then slid along the guide wire and coronary blood flow to the site of the coronary stenosis. MOA: reduces ischemic episodes by selective inhibition of The balloon is then inflated. The inflated balloon expands late sodium current the coronary lumen by stretching and tearing the Reduce cardiac oxygen demand, fatty acid oxidation atherosclerotic plaque. modification Stents are a stainless steel scaffold placed within coronary May improve efficiency of cardiac oxygen utilization arterials that can prevent acute vessel closure and Adverse effects from ranolazine use are constipation, restenosis. The stent is placed over the deflated balloon and nausea, dizziness, and headache. advanced to the area of coronary stenosis. When the balloon is inflated, the stent expands into the coronary Therapeutic doses ranolazine produces a modest vascular wall. The balloon is then deflated, leaving the prolongation of QTc (QTc means heart rate corrected QT expanded stent permanently in the diseased coronary interval) vessel. While ranolazine is safe and effective for treating angina episodes It would only be an option as monotherapy in patients with CORONARY ARTERY BYPASS GRAFTING SIHD who cannot tolerate traditional anti-angina agents Also known as Open Heart Surgery due to hemodynamic or other adverse effects. Once the heart is exposed, vascular conduits surgically Ranolazine is also recommended as add-on therapy to harvested from other areas of the body are used to traditional anti-angina agents. “bypass” the atherosclerotic plaque. ACC/AHA EVIDENCE GRADING SYSTEM ADDITIONAL FROM 2014 PHILIPPINE HEART ASSOCIATION Recommendation Class (COR) Level of Evidence (LOE) CLINICAL PRACTICE GUIDELINES FOR THE DIAGNOSIS AND Class I A. Multiple randomized clinical MANAGEMENT OF PATIENTS WITH STABLE ISCHEMIC Evidence or general agreement to trials, large no. of patients HEART DISEASE procedure or treatment is useful & effective B. Limited randomized clinical ACE INHIBITORS trials, small no. of patients, Class II careful analyses of are recommended for specific subgroups of patients with There is conflicting evidence or nonrandomized studies, or SIHD, such as those with: diverge opinions observational registries o coexisting HF or asymptomatic LV dysfunction (LVEF a. Weight of evidence or lower than 40%) opinion favors C. Expert; consensus was the o hypertension usefulness/efficacy primary basis of b. less well-established recommendation o or diabetes because of a reduction in the risk of future evidence to ischemic events. usefulness/efficacy Potential beneficial mechanisms of ACEIs include o regression in Left ventricular hypertrophy and vascular Class III Evidence or general agreement to hypertrophy procedures and treatment is not o prevention of atherosclerosis progression useful or effective. Some cases are o prevention of plaque rupture and thrombosis harmful o and a favorable influence in coronary endothelial Table above describes the ACC/AHA Class Recommendations (COR) and the Levels vasomotor function. Of Evidence (LOE). COR system, estimates the size of the treatment effect, balancing efficacy and safety. Each recommendation is also based on the LOE, NONPHARMACOLOGIC THERAPY which describes the quality, quantity and consistency of supporting data. REVASCULARIZATION Plays an important role in the treatment of SIHD. The most common revascularization procedures are coronary artery bypass grafting (CABG) surgery or percutaneous coronary intervention (PCI) with or without stent placement. The primary goal of revascularization is to prolong life and, to eliminate or reduce symptoms Whereas most of the pharmacologic approaches reduce myocardial volume oxygen consumption, revascularization  CANLAS, HAPITAN, MOSTAZA, RAMOS, SUBIJANO, SUGATAN, TEJARES | EBPT 1 8 TREATMENT ALGORITHM FOR STABLE ISCHEMIC HEART RISK FACTOR MODIFICATION: ACC/AHA DISEASE (GUIDELINE- DIRECTED MEDICAL THERAPY) RECOMMENDATIONS LIPID MANAGEMENT CLASS I Physical activity, diet and weight management Reduced intake of saturated fats, trans FA, cholesterol Pt without CI: High-intensity statin is prescribed Geriatrics (≥75 yo); Moderate intensity statin Addition of Ezetimibe or PCSK-9 inhibitor to px who cannot tolerate high-density statin or no 50% decrease in LDL Referral to lipid specialist is considered Saturated Fats