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The goals of therapy in chronic ischemic heart disease are to decrease the frequency of anginal attacks, to prevent acute coronary syndromes such as myocardial infarction, and to prolong survival.In addition, atherosclerosis-associated endothelial cell dysfunction causes inappropriate vasoconstriction of the coronary resistance vessels.New surgical techniques (increased use of various arterial grafts, less invasive operations); novel adjuncts to stenting (potent antithrombotic drugs, advanced approaches to prevent in-stent restenosis); and progress in pharmacologic management (e.g., aggressive use of statins and antithrombotic drugs) will likely further improve outcomes and better define the best therapeutic approaches for specific subsets of patients with chronic CAD.They relieve myocardial ischemia by (1) decreasing oxygen demand (vasodilatation reduces ventricular filling and size, arterial dilatation reduces the resistance against which the left ventricle contracts, and both actions reduce wall stress); and (2) increasing myocardial oxygen supply via coronary dilatation.However, care should be taken in combining a ?-blocker with a nondihydropyridine calcium channel blocker (verapamil or diltiazem) because the additive negative chronotropic effect can cause excessive bradycardia, and the combined negative inotropic effect could precipitate heart failure in patients with LV contractile dysfunction.That late phase tends to be abnormally enhanced in ischemic myocardium, and the associated increased sodium influx results in higher-than-normal intracellular Ca++ (mediated by the transsarcolemmal Na+-Ca++ exchanger; see Fig.Organic nitrates (e.g., nitroglycerin, isosorbide dinitrate, isosorbide mononitrate), as previously mentioned, relieve ischemia primarily through vasodilatation (i.e., lower

Ischemic Heart Disease 161 wall stress results from a smaller ventricular radius) and possibly through coronary vasodilatation.The benefits of statin therapy are believed to extend beyond their lipid-altering effects, because there is evidence that they decrease vascular inflammation and improve endothelial cell dysfunction and thus may help stabilize atherosclerotic plaques.Longer-acting anginal prevention can be achieved through a variety of nitrate preparations, including oral tablets of isosorbide dinitrate (or mononitrate) or a transdermal nitroglycerin patch, which is applied once a day.This medication has been shown to decrease the frequency of anginal episodes and improve exercise ca162 Chapter Six 10090-06_CH06.qxd 8/31/06 5:22 PM Page 162 Ischemic Heart Disease 163 pacity in patients with chronic CAD but differs from other anti-ischemic drugs in that it does not affect the heart rate or blood pressure.Aspirin has antithrombotic actions through inhibition of platelet aggregation (and therefore reduces the release of platelet-derived procoagulants and vasoconstrictors) as well as anti-inflammatory properties that may be important in stabilizing atheromatous plaque.Platelet aggregation o Gastrointestinal irritation or bleeding BP, blood pressure; D, diltiazem; LV, left ventricular; N, nifedipine and other dihydropyridine calcium++ channel antagonists; V, verapamil.The following sections describe medical
and surgical strategies to (1) reduce ischemia and its symptoms by restoring the balance between myocardial oxygen supply and demand, and (2) prevent acute coronary syndromes and death in patients with chronic CAD.(However, as described in Chapter 9, ?-blockers actually improve outcomes in patients with stable heart failure conditions.) ?- Blockers are also relatively contraindicated in patients with marked bradycardia or certain types of heart block to avoid additional impairment of electrical conduction.Moreover, although ?-blockers have demonstrated mortality benefits in patients after MI, none of has been shown to improve longevity in patients with chronic stable angina and preserved LV function.However, the combination of aspirin and cladogram is superior to aspirin alone in reducing death and ischemic complications in patients with acute coronary syndromes and in those undergoing elective percutaneous coronary stenting. All patients with CAD should have their LDL cholesterol maintained at 50%) stenosis of the left main coronary artery and patients with multivessel disease who also have reduced LV contractile function or diabetes.Improvements in other risk factors for CAD, including obesity and physical inactivity, are also likely to reduce the risk of adverse outcomes, although the benefits of these interventions
are less well documented.Consequently, ?-adrenergic antagonists decrease the force of ventricular contraction and heart rate, thereby relieving ischemia by reducing myocardial oxygen demand.In addition to suppressing angina, several studies have shown that ?-blockers decrease the rates of recurrent infarction and mortality following an acute MI (see Chapter 7).Although ?1-selective blockers are theoretically less likely to exacerbate bronchospasm in such patients, drug selectivity for the ?1- receptor is not complete, and in general, all ?-blockers should be avoided in patients with significant obstructive airway disease.However, these agents have additional beneficial antianginal effects stemming from their more potent cardiac depressant actions: they reduce the force of ventricular contraction (inotropy) and slow the heart rate.In particular, HMG-CoA reductase inhibitors (statins; see Chapter 17) lower MI and death rates in patients with established coronary disease and in those at high risk of developing CAD.They are directed against ?-receptors, of which there are two classes: ?1-adrenergic receptors are restricted to the myocardium, whereas ?2-adrenergic receptors are located throughout blood vessels and the bronchial tree.One might also expect that ?-blockers would decrease myocardial blood perfusion by blocking the vasodilating ?2-adrenergic receptors on the coronary arteries.Medical Treatment to Prevent Acute Cardiac Events Platelet aggregation and thrombosis are key elements in the pathophysiology of acute MI and unstable angina (see Chapter 7).As described in Chapter 17, they irreversibly bind to the platelet ADP receptor P2Y12, thereby preventing platelet activation and aggregation.Data convincingly demonstrate the benefit of smoking cessation, cholesterol reduction, blood pressure control, and serum glucose control in lowering the risk of coronary disease events (see Chapter 5).In addition, when taken immediately before a person engages in activities known to provoke angina, these rapidly acting nitrates are useful as prophylaxis against anginal attacks.A limitation to chronic nitrate therapy is the development of drug tolerance (i.e., decreased effectiveness of the drug during continued administration), which occurs to some degree in most patients.?-Blockers are also generally not used in patients with acutely decompensated LV dysfunction because they could intensify heart failure symptoms by further reducing inotropy.No dihydropyridine calcium channel blockers (verapamil and diltiazem) also act as vasodilators but are not as potent in this regard as the dihydropyridines.In meta-analyses of randomized trials, these drugs have been associated with an increased incidence of MI and mortality.Pending further studies and experience, ranolazine is currently approved only for patients who have not responded adequately to the standard antianginal drugs described earlier.Preload (vasodilatation) o Hypotension o Reflex tachycardia ?1.10).2.


النص الأصلي

The goals of therapy in chronic ischemic heart disease are to decrease the frequency of anginal attacks, to prevent acute coronary syndromes such as myocardial infarction, and to prolong survival. A long-term crucial step is to address the risk factors that led to the development of atherosclerotic coronary
disease. Data convincingly demonstrate the benefit of smoking cessation, cholesterol reduction, blood pressure control, and serum glucose control in lowering the risk of coronary disease events (see Chapter 5). Improvements in other risk factors for CAD, including obesity and physical inactivity, are also likely to reduce the risk of adverse outcomes, although the benefits of these interventions
are less well documented. The following sections describe medical
and surgical strategies to (1) reduce ischemia and its symptoms by restoring the balance between myocardial oxygen supply and demand, and (2) prevent acute coronary syndromes and death in patients with chronic CAD. Medical Treatment of an Acute Episode of Angina When experiencing angina, the patient should cease physical activity. Sublingual nitroglycerin, an organic nitrate, is the drug of choice in this situation. Placed under the tongue, this medication produces a slight burning sensation as it is absorbed through the mucosa, and it begins to take effect in 1 to 2 minutes. Nitrates relieve ischemia primarily through vascular smooth muscle relaxation, particularly vasodilatation. Vasodilatation reduces venous return to the heart, with a subsequent decline in LV volume (a determinant of wall stress). The latter decreases myocardial oxygen consumption, thus helping to restore oxygen balance in the ischemic heart. A second action of nitrates is to dilate the coronary vasculature, with subsequent augmentation of coronary blood flow. This effect
may be of minimal value in patients with angina in whom maximal coronary dilatation has already resulted from the accumulation of local metabolites. However,
when coronary vasospasm plays a role in the development of ischemia, nitrate-induced coronary vasodilatation may be particularly
beneficial. Medical Treatment to Prevent Recurrent Ischemic Episodes Pharmacologic agents are also the first line of defense in the prevention of anginal attacks. The goal of these agents is to decrease the cardiac workload (i.e., reduce myocardial oxygen demand) and to increase myocardial perfusion. The three classes of medications commonly used are the organic
nitrates, β-adrenergic blockers, and calcium channel blockers (Table 6.3). Organic nitrates (e.g., nitroglycerin, isosorbide dinitrate, isosorbide mononitrate), as previously mentioned, relieve ischemia primarily through vasodilatation (i.e., lower


Ischemic Heart Disease 161 wall stress results from a smaller ventricular radius) and possibly through coronary vasodilatation. The organic nitrates are the oldest of the antianginal drugs and come in several preparations. Sublingual nitroglycerin tablets or sprays are used in the treatment of acute attacks because of their rapid onset of action. In addition, when taken immediately before a person engages in activities known to provoke angina, these rapidly acting nitrates are useful as prophylaxis against anginal attacks. Longer-acting anginal prevention can be achieved through a variety of nitrate preparations, including oral tablets of isosorbide dinitrate (or mononitrate) or a transdermal nitroglycerin patch, which is applied once a day. A limitation to chronic nitrate therapy is the development of drug tolerance (i.e., decreased effectiveness of the drug during continued administration), which occurs to some degree in most patients. This undesired effect can be overcome by providing a nitrate-free interval for several hours each day, usually while the patient sleeps. There is no evidence that nitrates improve survival or prevent infarctions in patients with chronic CAD, and they are used purely for symptomatic relief. Common side effects include headache, lightheadedness, and palpitations induced by reflex sinus tachycardia. The latter can be prevented by combining a β-blocker with the nitrate regimen. -Blockers (see Chapter 17) exert their antianginal effect primarily by reducing myocardial oxygen demand. They are directed against β-receptors, of which there are two classes: β1-adrenergic receptors are restricted to the myocardium, whereas β2-adrenergic receptors are located throughout blood vessels and the bronchial tree. The stimulation of β1-receptors by endogenous catecholamines and exogenous sympathomimetic drugs increases heart rate and contractility. Consequently, β-adrenergic antagonists decrease the force of ventricular contraction and heart rate, thereby relieving ischemia by reducing myocardial oxygen demand. In addition, slowing the heart rate may benefit myocardial oxygen supply by augmenting the TABLE 6.3. Pharmacologic Agents in the Treatment of Angina Drug Class Mechanism of Action Adverse Effects Organic nitrates ↓ Myocardial O2 demand • Headache ↓ Preload (vasodilatation) • Hypotension • Reflex tachycardia ↑ O2 supply ↑ Coronary perfusion ↓ Coronary vasospasm β-blockers ↓ Myocardial O2 demand • Excessive bradycardia ↓ Contractility • ↓ LV contractile function ↓ Heart rate • Bronchoconstriction • May worsen diabetic control • Fatigue Calcium channel blockers ↓ Myocardial O2 demand • Headache, flushing (agent specific; see footnote) ↓ Preload (vasodilatation) ↓ LV contraction (V, D) ↓ Wall stress (↓BP) • Marked bradycardia (V, D) ↓ Contractility (V, D) • Edema (especially N, D) ↓ Heart rate (V, D) • Constipation (especially V) ↑ O2 supply ↑ Coronary perfusion ↓ Coronary vasospasm Aspirin ↓ Platelet aggregation • Gastrointestinal irritation or bleeding BP, blood pressure; D, diltiazem; LV, left ventricular; N, nifedipine and other dihydropyridine calcium++ channel antagonists; V, verapamil. 10090-06_CH06.qxd 8/31/06 5:22 PM Page 161 time spent in diastole, the phase when coronary perfusion primarily occurs. In addition to suppressing angina, several studies have shown that β-blockers decrease the rates of recurrent infarction and mortality following an acute MI (see Chapter 7). Moreover, they have been shown to reduce the likelihood of an initial MI in patients with hypertension. Thus, β-blockers are first-line therapy in the treatment of CAD. β-Blockers are generally well tolerated but have several potential side effects. For example, they may precipitate bronchospasm in patients with underlying asthma by antagonizing β2-receptors in the bronchial tree. Although β1-selective blockers are theoretically less likely to exacerbate bronchospasm in such patients, drug selectivity for the β1- receptor is not complete, and in general, all β-blockers should be avoided in patients with significant obstructive airway disease. β-Blockers are also generally not used in patients with acutely decompensated LV dysfunction because they could intensify heart failure symptoms by further reducing inotropy. (However, as described in Chapter 9, β-blockers actually improve outcomes in patients with stable heart failure conditions.) β- Blockers are also relatively contraindicated in patients with marked bradycardia or certain types of heart block to avoid additional impairment of electrical conduction. β-Blockers sometimes cause fatigue and sexual dysfunction. They should be used with caution in insulin-treated diabetic patients because they can mask tachycardia and other catecholamine-mediated responses that can warn of hypoglycemia. One might also expect that β-blockers would decrease myocardial blood perfusion by blocking the vasodilating β2-adrenergic receptors on the coronary arteries. However, this effect is usually attenuated by autoregulation and vasodilation of the coronary vessels owing to the accumulation of local metabolites. Calcium channel blockers (see Chapter 17) antagonize voltage-gated L-type calcium channels, but the actions of the individual drugs of this group vary. The dihydropyridines (e.g., nifedipine and amlodipine) are potent vasodilators. They relieve myocardial ischemia by (1) decreasing oxygen demand (vasodilatation reduces ventricular filling and size, arterial dilatation reduces the resistance against which the left ventricle contracts, and both actions reduce wall stress); and (2) increasing myocardial oxygen supply via coronary dilatation. By the latter mechanism, they are also potent agents for the relief of coronary artery vasospasm. No dihydropyridine calcium channel blockers (verapamil and diltiazem) also act as vasodilators but are not as potent in this regard as the dihydropyridines. However, these agents have additional beneficial antianginal effects stemming from their more potent cardiac depressant actions: they reduce the force of ventricular contraction (inotropy) and slow the heart rate. Accordingly, verapamil and diltiazem also decrease myocardial oxygen demand by these mechanisms. Questions have been raised about the safety of short-acting calcium channel–blocking drugs in the treatment of ischemic heart disease. In meta-analyses of randomized trials, these drugs have been associated with an increased incidence of MI and mortality. The adverse effect may relate to the rapid hemodynamic effects and blood pressure swings induced by the short-acting agents. Therefore, only long-acting calcium channel blockers are recommended in the treatment of chronic angina, generally as second-line drugs if symptoms are not controlled by β-blockers and nitrates. The three standard groups of antianginal drugs described in this section can be used alone or in combination. However, care should be taken in combining a β-blocker with a nondihydropyridine calcium channel blocker (verapamil or diltiazem) because the additive negative chronotropic effect can cause excessive bradycardia, and the combined negative inotropic effect could precipitate heart failure in patients with LV contractile dysfunction. In 2006, the Food and Drug Administration approved ranolazine, a fourth type of anti-ischemic therapy. This medication has been shown to decrease the frequency of anginal episodes and improve exercise ca162 Chapter Six 10090-06_CH06.qxd 8/31/06 5:22 PM Page 162 Ischemic Heart Disease 163 pacity in patients with chronic CAD but differs from other anti-ischemic drugs in that it does not affect the heart rate or blood pressure. Although its mechanism of action has not been fully elucidated, it is believed to inhibit the late phase of the action potential’s inward sodium current (INa+) in ventricular myocytes. That late phase tends to be abnormally enhanced in ischemic myocardium, and the associated increased sodium influx results in higher-than-normal intracellular Ca++ (mediated by the transsarcolemmal Na+-Ca++ exchanger; see Fig. 1.10). This calcium overload is thought to result in impaired diastolic relaxation (i.e., diastolic dysfunction; see Chapter 9) and contractile inefficiency. Inhibition of the late INa+ by ranolazine counters these pathologic effects. Pending further studies and experience, ranolazine is currently approved only for patients who have not responded adequately to the standard antianginal drugs described earlier. Although useful in controlling symptoms of angina, none of the antianginal drug groups has been shown to slow or reverse the atherosclerotic process responsible for the arterial lesions of chronic CAD. Moreover, although β-blockers have demonstrated mortality benefits in patients after MI, none of has been shown to improve longevity in patients with chronic stable angina and preserved LV function. Medical Treatment to Prevent Acute Cardiac Events Platelet aggregation and thrombosis are key elements in the pathophysiology of acute MI and unstable angina (see Chapter 7). Antiplatelet therapy reduces the risk of these acute coronary syndromes in patients with chronic angina and should be a standard part of the regime used to treat CAD. Aspirin has antithrombotic actions through inhibition of platelet aggregation (and therefore reduces the release of platelet-derived procoagulants and vasoconstrictors) as well as anti-inflammatory properties that may be important in stabilizing atheromatous plaque. Unless contraindications are present (e.g., allergy or gastric bleeding), aspirin should be continued indefinitely in all patients with CAD. Thienopyridines, including copylore, compose another group of antiplatelet agents. As described in Chapter 17, they irreversibly bind to the platelet ADP receptor P2Y12, thereby preventing platelet activation and aggregation. When compared with aspirin in clinical trials of patients with stable atherosclerotic disease, cladogram resulted in only a modest reduction of cardiovascular events. However, the combination of aspirin and cladogram is superior to aspirin alone in reducing death and ischemic complications in patients with acute coronary syndromes and in those undergoing elective percutaneous coronary stenting. Lipid-regulating therapy also reduces cardiovascular clinical events. In particular, HMG-CoA reductase inhibitors (statins; see Chapter 17) lower MI and death rates in patients with established coronary disease and in those at high risk of developing CAD. The benefits of statin therapy are believed to extend beyond their lipid-altering effects, because there is evidence that they decrease vascular inflammation and improve endothelial cell dysfunction and thus may help stabilize atherosclerotic plaques. All patients with CAD should have their LDL cholesterol maintained at 50%) stenosis of the left main coronary artery and patients with multivessel disease who also have reduced LV contractile function or diabetes. Each of the previously described approaches for the treatment of coronary disease is benefiting from rapidly developing research advancements. New surgical techniques (increased use of various arterial grafts, less invasive operations); novel adjuncts to stenting (potent antithrombotic drugs, advanced approaches to prevent in-stent restenosis); and progress in pharmacologic management (e.g., aggressive use of statins and antithrombotic drugs) will likely further improve outcomes and better define the best therapeutic approaches for specific subsets of patients with chronic CAD. SUMMARY 1. Cardiac ischemia results from an imbalance between myocardial oxygen supply and demand. Myocardial oxygen supply is determined by the oxygen content of the blood and coronary blood flow. The latter is dependent on the coronary perfusion pressure and coronary vascular resistance. Key regulators of myocardial oxygen demand include myocardial wall stress, heart rate, and contractility. 2. In the presence of atherosclerotic disease, myocardial oxygen supply is compromised. Atherosclerotic plaques cause vascular lumen narrowing and reduce coronary blood flow. In addition, atherosclerosis-associated endothelial cell dysfunction causes inappropriate vasoconstriction of the coronary resistance vessels.


تلخيص النصوص العربية والإنجليزية أونلاين

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