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The Big Heart Disease Lie

Cardiovascular Disease Homeopathic Treatments

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Family history of premature cardiovascular disease, defined as cardiovascular disease in a male first-degree relative (i.e., father or brother) younger than 55 year:-, old or a female first-degree relative (i.e., mother or sister) younger than 65 years

HDL. high density lipoprotein; LDL, low density lipoprotein.

Patients with multiple risk factors, particularly those with diabetes, are at the greatest risk for IHD. While there are alternative definitions for metabolic syndrome, it is generally considered as a constellation of cardiovascular risk factors related to hypertension, abdominal obesity, dyslipidemia, and insulin resistance. Metabolic syndrome increases the risk of developing IHD and related complications by twofold.6 According to the American Heart Association, patients must meet at least three of the following criteria for the diagnosis of metabolic syndrome :

• Increased waist circumference (more than or equal to 40 inches or 102 centimeters in males and more than or equal to 35 inches or 89 centimeters in females).

• Triglycerides of 150 mg/dL (1.70 mmol/L) or greater or active treatment to lower triglycerides.

• Low high-density lipoprotein (HDL) cholesterol (less than 40 mg/dL or 1.04 mmol/L in males and less than 50 mg/dL or 1.3 mmol/L in females) or active treatment to raise HDL cholesterol.

• Systolic blood pressure of 130 mm Hg or greater, diastolic blood pressure of 85 mm Hg or greater, or active treatment with antihypertensive therapy.

• Fasting blood glucose of 100 mg/dL (5.55 mmol/L) or greater or active treatment for diabetes.

Early detection and aggressive modification of riskfactors are among the primary strategies for delaying IHD progression and preventing IHD-related events including death.

PATHOPHYSIOLOGY

The determinants of oxygen supply and demand are shown in Figure 7-1. Increases in heart rate, cardiac contractility, and left ventricular wall tension increase the rate of myocardial oxygen consumption (MVO2). Ventricular wall tension is a function of blood pressure, left ventricular end-diastolic volume, and ventricular wall thickness. Physical exertion increases MVO2 and commonly precipitates symptoms of angina in patients with significant coronary atherosclerosis. Medications that reduce heart rate, cardiac contractility, and/or ventricular wall tension are commonly prescribed to prevent ischemic symptoms in chronic stable angina.

Reductions in coronary blood flow (secondary to atherosclerotic plaques, vasospasm, or thrombus formation) and arterial oxygen content (secondary to hypoxia) decrease myocardial oxygen supply. Because the coronary arteries fill during diastole, decreases in diastolic filling time (e.g., tachycardia) can also reduce coronary perfusion and myocardial oxygen supply. In chronic stable angina, atherosclerotic plaques are the most common cause of coronary artery narrowing and reductions in coronary blood flow. In contrast, in ACS, disruption of an atherosclerotic plaque with subsequent thrombus (blood clot) formation causes abrupt reductions in coronary blood flow and oxygen supply. Anemia, carbon monoxide poisoning, and cyanotic congenital heart disease are examples of conditions that reduce the oxygen-carrying capacity of the blood, potentially causing ischemia in the face of adequate coronary perfusion. Interventional procedures to compress, cut away, or bypass atherosclerotic plaques are effective methods of improving myocardial oxygen supply in patients with IHD.

Coronary Atherosclerosis

The normal arterial wall is illustrated in Figure 7-3A. The intima consists of a layer of endothelial cells that line the lumen of the artery and form a selective barrier between the vessel wall and blood contents. Vascular smooth muscle cells are found in the media. The vascular adventitia comprises the artery's outer layer. Atherosclerotic lesions form in the subendothelial space in the intimal layer.

Endothelial dysfunction allows low-density lipoprotein (LDL) cholesterol and inflammatory cells (e.g., monocytes and T lymphocytes) to migrate from the plasma to the subendothelial space, as illustrated in Figure 12-5 in the Dyslipidemias chapter. Monocyte-derived macrophages ingest lipoproteins to form foam cells. Macrophages also secrete growth factors that promote smooth muscle cell migration from the media to the intima. A fatty streak consisting of lipid-laden macrophages and smooth muscle cells is formed. The fatty streak is the earliest type of atherosclerotic lesion.

The fatty streak enlarges as foam cells, smooth muscle cells, and necrotic debris accumulate in the subendothelial space. A collagen matrix forms a fibrous cap that covers the lipid core of the lesion to establish an atherosclerotic plaque. The atherosclerotic plaque may progress until it protrudes into the artery lumen and impedes blood flow. When the plaque occludes 70% or more of a major coronary artery or 50% or more of the left main coronary artery, the patient may experience angina during activities that increase myocardial oxygen demand.

Stable Versus Unstable Atherosclerotic Plaques

The hallmark feature in the pathophysiology of chronic stable angina is an established atherosclerotic plaque that impedes coronary blood flow to the extent that myocardial oxygen supply can no longer meet increases in myocardial oxygen demand. In contrast, the hallmark feature in the pathophysiology of ACS is atherosclerotic plaque rupture with subsequent thrombus formation. Plaque rupture refers to Assuring of the fibrous cap and exposure of the plaque contents to elements in the blood. Plaque composition, rather than the degree of coronary stenosis, determines the stability of the plaque and the likelihood of rupture and ACS. As depicted in Figure 7-3B, a stable lesion characteristic of chronic stable angina consists of a small lipid core that is surrounded by a thick fibrous cap that protects the lesion from the shear stress of blood flow. In contrast, an unstable plaque consists of a thin, weak cap in combination with a large, rich lipid core that renders the plaque vulnerable to rupture (Fig. 7-3C). The transformation of a stable plaque into an unstable plaque involves the degradation of the fibrous cap by substances released from macrophages and other inflammatory cells. Following plaque rupture, platelets adhere to the site of rupture, aggregate, and generate thrombin and a fibrin clot (Fig. 7-3D-F). Coronary thrombi extend into the vessel lumen, where they either partially or completely occlude blood flow, resulting in unstable angina or ML.

Chronic stable angina

Smoc Blood Clot

Smooth muscle cells

Coronary artery lumen

Endothelium Coronary artory lumen internal elastic / lamina

Advenu ta

Smoc<h muscle eel»

Coronary artery m lumen

Coronary artory lumen intima

Media

Med a

Advent it la

Smooth muscle cells

Smooth muscle cete

Platelet weiten

Media

Smooth muscle eels

I Normal coronary

Endothetel cells

intima • Adventiiio

Acute coronary syndrome

Plaque fiSSu'ft' rupture

Stable AineroKleitfK pteqoe lipo core

Strwom mwsde cells lipdcco

Lipid core

Leid core

FIGURE 7-3. Pathophysiology of chronic stable angina versus acute coronary syndromes. A depicts the cross section of a normal coronary artery. B depicts the cross section of a coronary artery with a stable atherosclerotic plaque. Note that the lipid core is relatively small in size and the fibrous cap is made up of several layers of smooth muscle cells. C depicts an unstable atherosclerotic plaque with a larger lipid core, and a thin fibrous cap comprised of a single layer of smooth muscle cells with a fissure or rupture. D depicts platelet adhesion in response to the fissured plaque. Platelet activation may ensue leading to platelet aggregation as fibrinogen binds platelets to one another to form a meshlike occlusion in the coronary lumen (E). At this stage, patients may experience symptoms of acute coronary syndrome. If endogenous anticoagulant proteins fail to halt this process, platelet aggregation continues and fibrinogen is converted to fibrin, resulting in an occlusive thrombus (F).

An unstable plaque often produces minimal occlusion of the coronary vessel, and the patient remains asymptomatic until the plaque ruptures. In fact, the majority of MIs arise from vulnerable plaques that occlude less than 50% of the coronary lumen.8 As a result, unstable angina or MI is the initial manifestation of IHD in about one-half of affected patients.

Coronary Artery Vasospasm

Prinzmetal or variant angina results from spasm (or contraction) of a coronary artery in the absence of significant atherosclerosis. Variant angina usually occurs at rest, especially in the early morning hours. While vasospasm is generally transient, in some instances vasospasm may persist long enough to infarct the myocardium. Patients with variant angina are typically younger than those with chronic stable angina and often do not possess the classic risk factors for IHD. The cause of variant angina is unclear but appears to involve endothelial dysfunction and paradoxical response to agents that normally cause vasodilation. Precipitants of variant angina include cigarette smoking, cocaine use, hyperventilation, and exposure to cold temperatures. The management of variant angina differs from that of classic angina, and thus it is important to distinguish between the two.

CLINICAL PRESENTATION AND DIAGNOSIS History

The evaluation of a patient with suspected IHD begins with a detailed history of symptoms. The classic presentation of angina is described in the Clinical Presentation and Diagnosis box. Chronic stable angina should be distinguished from unstable angina since the latter is associated with a greater risk for MI and death and requires more aggressive treatment. Because the pathophysiology of chronic stable angina is due primarily to increases in oxygen demand, rather than acute changes in oxygen supply, symptoms are typically reproducible. Specifically, a patient with angina secondary to significant coronary atherosclerosis will generally experience a similar pattern of discomfort (i.e., same quality, location, and accompanying symptoms) with a similar level of exertion with each angina attack. The exception maybe a patient with coronary artery vasospasm, in whom symptoms maybe more variable and unpredictable. In contrast to chronic stable angina, ACS is due to an acute decrease in coronary blood flow leading to insufficient oxygen supply. Consequently, ACS is marked by prolonged symptoms, symptoms that occur at rest, or an escalation in the frequency or severity of angina over a short period of time. The presentation of unstable angina is described in Table 7-3.9

Clinical Presentation and Diagnosis of Ischemic Heart Disease

General

• Patients with chronic stable angina will generally be in no acute distress. In patients presenting in acute distress, the clinician should be suspicious of ACS.

Symptoms of Angina Pectoris

• The five components commonly used to characterize chest pain are quality, location, and duration of pain; factors that provoke pain; and factors that relieve pain.

• Patients typically describe pain as a sensation of pressure, heaviness, or squeezing in the anterior chest area. Sharp pain is not a typical symptom of IHD.

• Pain may radiate to the neck, jaw, shoulder, back, or arm.

• Pain may be accompanied by dyspnea, nausea, vomiting, or diaphoresis.

• Symptoms are often provoked by exertion (e.g., walking, climbing stairs, and doing yard-or housework) or emotional stress and relieved within minutes by rest or sublingual nitroglycerin. Other precipitating factors include exposure to cold temperatures and heavy meals. Pain that occurs at rest (without provocation) or that is prolonged and unrelieved by sublingual nitroglycerin is indicative of an ACS.

• Some patients, most commonly women and patients with diabetes, may present with atypical symptoms including indigestion, gastric fullness, and shortness of breath. Patients with diabetes may experience associated symptoms, such as dyspnea and diaphoresis, without having any of the classic chest pain symptoms

• In some cases, ischemia may not produce any symptoms and is termed "silent ischemia."

Signs

• Findings on the physical exam are often normal in patients with chronic stable angina. However, during episodes of ischemia, patients may present with abnormal heart sounds, such as paradoxical splitting of the second heart sound, a third heart sound, or a loud fourth heart sound.

Laboratory Tests

• Cardiac enzymes (creatine kinase [CK], CK-MB fraction, troponin I and troponin T) are elevated in Ml (ST-segment elevation Ml and non-ST-segment elevation Ml), but normal in chronic stable angina and unstable angina.

• Hemoglobin, fasting glucose, and fasting lipid profile should be determined for assessing cardiovascular risk factors and establishing the differential diagnosis.

Other Diagnostic Tests

• A 12-lead ECG recorded during rest is often normal in patients with chronic stable angina in the absence of active ischemia. Significant Q waves indicate prior Ml. ST-segment or T-wave changes in two or more contiguous leads during symptoms of angina support the diagnosis of IHD. ST-segment depression or T-wave inversion is typically observed in chronic stable angina, unstable angina, and non-ST-segment elevation Ml, whereas ST-segment elevation occurs with ST-segment elevation Ml and Prinzmetal (variant) angina.

Treadmill or bicycle exercise ECG, commonly referred to as a "stress test," is considered positive for IHD if the ECG shows at least a 1 mm deviation of the ST-seg-ment (depression or elevation).

• Wall motion abnormalities or left ventricular dilation with stress echocardiography are indicative of IHD.

• Stress myocardial perfusion imaging with the radionuclides technetium-99m ses-tamibi or thallium-201 allows for the identification of multivessel disease and assessment of myocardial viability.

• Coronary angiography detects the location and degree of coronary atherosclerosis and is used to evaluate the potential benefit from revascularization procedures. Stenosis of at least 70% of the diameter of at least one of the major epicardial arteries on coronary angiography is indicative of significant IHD.

The Canadian Cardiovascular Society Classification System

The Canadian Cardiovascular Society Classification System (Table 7-4) is commonly used to assess the degree of disability resulting from IHD.10 Patients are categorized into one of four classes depending on the extent of activity that produces angina. Grouping patients according to this or a similar method is commonly used to assess changes in IHD severity over time and the effectiveness of pharmacologic therapy.

Physical Findings and Laboratory Analysis

A thorough medical history, physical exam, and laboratory analysis are necessary to ascertain cardiovascular risk factors and to exclude nonischemic and noncardiac conditions that could cause angina-like symptoms. Laboratory analyses should assess for glycemic control (i.e., fasting glucose, glycosylated hemoglobin), fasting lipids, hemoglobin, and organ function (i.e., blood urea nitrogen, creatinine, liver function tests, thyroid function tests). Additionally, serial measurements of cardiac enzymes (usually three measurements within 24 hours) are used to exclude the diagnosis of MI. Cardiac findings on the physical exam are often normal in patients with chronic stable angina. However, findings such as carotid bruits or abnormal peripheral pulses would indicate atherosclerosis in other vessel systems and raise the suspicion for IHD.

Table 7-3 Presentations of Acute Coronary Syndromes

• Angina at rest that is prolonged in duration, usually lasting over 20 minutes

• Angina of recent onset (within 2 months) that markedly limits usual activity

• Angina that increases in severity (i.e., by Canadian Cardiovascular Society Classification System of one level or more), frequency, or duration, or that occurs with less provocation over a short time period (i.e., within 2 months)

Table 7-4 The Canadian Cardiovascular Society Classification System of Angina

Cla$$ Description

I Able to perform ordinary physical activity {e.g., walking and climbing stairs) without symptoms. Strenuous, rapid, or prolonged exertion causes symptoms

II Sy m ptoms slightly limit ordinary physical act i vi ty.

Walking rapidly or for more Than two blocks, climbing stairs rapidly or climbing more than one flight of stairs causes symptoms

III Symptoms markedly limit ordinary physical activity.

Walking less than two blocks or climbing one flight of stairs causes symptoms

IV Angina may occur at rest. Any physical activity causes symptoms

Patient Encounter, Part 1

RJ is a 47-year-old man with a history of hypertension who presents to your clinic complaining of chest pain that occurred several times over the past few weeks. RJ describes his chest pain as "a heaviness." He states that it first occurred while he was mowing the grass. He later felt the same heavy sensation while raking leaves and again while carrying some boxes. The pain was located in the substernal area and radiated to his neck. The pain resolved after about 5 minutes of rest.

What information is suggestive of angina?

What tests would be beneficial in establishing a diagnosis?

What additional information do you need to create a treatment plan for this patient? Diagnostic Tests

A resting ECG is indicated in all patients with angina-like symptoms. A 12-lead ECG should be done within 10 minutes of presentation to the emergency department in patients with symptoms of ischemia. Patients with ST-segment elevation are at the highest risk of death and need interventions to restore blood flow to the myocardium as quickly as possible. In patients without ST-segment elevation, biochemical markers are used to distinguish between unstable angina and non-ST-segment elevation MI.

"Stress" testing with either exercise or pharmacologic stressors increases myocar-dial oxygen demand and is commonly used to evaluate the patient with suspected IHD. Approximately 50% of patients with IHD who have a normal ECG at rest will develop ECG changes with exercise on a treadmill (most commonly) or bicycle ergometer. Dobutamine is a pharmacologic stressor used in patients who are unable to exercise. Dobutamine increases oxygen demand by stimulating the P1-receptor, leading to increases in heart rate and contractility. Dobutamine is commonly used with echocardiography (referred to as dobutamine stress echocardiography) to identify stress-induced wall motion abnormalities indicative of coronary disease.

Adenosine and dipyridamole are coronary vasodilators commonly combined with radionuclide myocardial perfusion imaging (nuclear imaging studies). These agents increase coronary blood flow in vessels free of disease, but not in diseased vessels. An IV radioactive tracer is used to detect areas of the heart that receive less blood after adenosine or dipyridamole infusion, indicating a myocardial perfusion defect and coronary disease.

Coronary artery calcium scoring via CT, also known as electron beam CT (EBCT) or "ultra-fast CT," may be performed as a noninvasive means to assess for IHD. Calcium deposits within the coronary arteries which are indicative of IHD are detected on CT. A calcium score is calculated, and the risk for IHD-related events is estimated.

Coronary angiography (also referred to as a cardiac catheterization or "cardiac cath") is considered the gold standard for the diagnosis of IHD. Coronary angio-graphy is indicated when stress testing results are abnormal or symptoms of angina are poorly controlled. Angiography involves catheter insertion, usually into the femoral artery, and advancement into the aorta and into the coronary arteries. Contrast medium is injected through the catheter into the coronary arteries allowing visualization of the coronary anatomy by fluoroscopy. Contrast medium must be used cautiously with adequate hydration in patients with pre-existing renal disease (especially in those with diabetes) to avoid contrast-induced nephropathy.

TREATMENT

Desired Outcomes

Once the diagnosis of IHD is established in a patient, the clinician should provide counseling on lifestyle modifications, institute appropriate pharmacologic therapy, and evaluate the need for surgical revascularization. The major goals for the treatment of IHD are to:

• Prevent ACSs and death

• Alleviate acute symptoms of myocardial ischemia

• Prevent recurrent symptoms of myocardial ischemia

• Avoid or minimize adverse treatment effects

The treatment approach to address these goals is illustrated in Figure 7-4.

Patient Encounter, Part 2: Medical History, Physical Exam, and Diagnostic Tests PMH: Hypertension, diagnosed 7 years ago

FH: Father with coronary artery disease, had a myocardial infarction at age 50 years; mother alive and well

SH: Smokes half a pack to a pack per day; denies alcohol and illicit drug use; no regular exercise program

Allergies: NKDA

Meds: Hydrochlorothiazide 25 mg orally once daily; nifedipine XL 60 mg orally once daily

VS: BP 154/90 mm Hg, HR 84 bpm, RR 16 per minute, T 37°C (98.6°F), Ht 5'10" (178 cm), wt 105 kg (230 lb)

CV: RRR, normal Si and S2, no S3 or S4; no murmurs, rubs, gallops Lungs: Clear to auscultation and percussion Abd: Nontender, nondistended, + bowel sounds

Labs: Fasting lipid profile: total cholesterol 233 mg/dL (6.03 mmol/L), HDL cholesterol 30 mg/dL (0.78 mmol/L), LDL cholesterol 165 mg/dL (4.27 mmol/L), triglycerides 188 mg/dL (2.12 mmol/L); other labs within normal limits

Exercise treadmill test: Positive for ischemia

Identify RJ's risk factors for ischemic heart disease.

How might RJ's current drug regimen adversely affect his ischemic heart disease? What therapeutic alternatives are available to manage RJ's IHD?

General Approach to Treatment

The primary strategies for preventing ACS and death are to:

• Modify cardiovascular risk factors

• Slow the progression of coronary atherosclerosis

• Stabilize existing atherosclerotic plaques

The treatment algorithm in Figure 7-5 summarizes the appropriate management of IHD. Risk factor modification is accomplished through lifestyle changes and pharmacologic therapy. Both 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (HMG-CoA reductase inhibitors or statins) and angiotensin-converting enzyme (ACE) inhibitors are believed to provide vasculoprotective effects (properties that are generally protective of the vasculature, which may include anti-inflammatory effects, antiplatelet effects, improvement in endothelial function, and improvement in arterial compliance and tone), and in addition to aspirin, have been shown to reduce the risk of acute coronary events as well as mortality in patients with IHD. Angiotensin receptor blockers (ARBs) may be used in patients who cannot tolerate ACE inhibitors because of side effects (e.g., chronic cough). fi-Blockers have been shown to decrease morbidity and improve survival in patients who have suffered an MI.

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