Calcium-Channel Blockers in Anginal Syndromes
Amlodipine Angina, hypertension 2.5–10 mg every day 2.5, 5, 10 mg tab
Felodipine Hypertension 5–20 mg every day 5, 10 mg ER tab
Isradapine Hypertension 2.5–10 mg BID 2.5, 5 mg IR cap
5–10 mg every day 5, 10 mg CR tab
30–60 mg BID 30, 45, 60 mg SR cap
Nifedipine Angina, hypertension 10–30 mg TID 10, 20 mg IR cap
30–180 mg every day 30, 60, 90 mg ER tab
Nisoldipine Hypertension 20–60 mg every day 10, 20, 30, 40 mg ER tab
Verapamil Angina, hypertension,
30–120 mg TID/QID 40, 80, 120 mg IR tab
120–240 mg BID 120, 180, 240 mg SR tab
120–480 mg every HS 180, 240 mg DR, ER tab
Diltiazem Angina, hypertension,
30–120 mg TID/QID 30, 60, 90, 120 mg IR tab
60–180 mg BID 60, 90, 120, 180 mg SR
120–480 mg every day 120, 180, 240, 300, 360 mg
angina and hypertension. Avoid IR products in hypertension.
half-life and is given once daily.
tablets; TID, three times a day.
Despite the availability of data regarding the relative effects of PCI, CABG, and
medical management on morbidity and mortality, there has been a dramatic increase
in the use of PCI in recent years. CABG remains the preferred strategy for patients
with three-vessel disease or who have multi-vessel disease plus left ventricular
dysfunction. In patients with less severe CAD, PCI can be expected to provide
similar benefits in mortality as compared to CABG, but may not be as effective at
reducing symptoms or the need for repeat revascularization procedures. Recent
investigations have indicated that aggressive medical treatment, including intensive
lipid-lowering therapy, may be as effective as PCI at improving prognosis over the
long term, but may be inferior at reducing symptoms of angina.
significant in that they highlight the importance of implementing effective strategies,
which reduce the progression of CAD, regardless of whether revascularization
therapy is utilized. Relevant issues facing pharmacists today not only include
optimizing the medical management of CAD but also providing effective
pharmacotherapy to prevent complications of PCI.
CLINICAL PRESENTATION OF CHRONIC
or a particular time of day. When J.P. stops working, the pain subsides in about 5 minutes.
age 86, has survived one heart attack and one stroke. Family history (except for J.P.)
beers a day and does not smoke or chew tobacco.
cheeseburgers and French fries.
of 84 beats/minute without evidence of previous MI. All intervals are within normal limits.
Admitting laboratory values include the following:
White blood cell (WBC) count, 5,000/μL
Random blood glucose, 132 mg/dL
Urinary albumin–creatinine ratio, 27 mg/mmol
Chest radiograph is within normal limits.
J.P.’s description of his chest pain includes several common characteristics of
1–3 The substernal location of J.P.’s chest pain is
typical, although some patients describe pain radiating down the left arm or pain that
is referred to the shoulder area or jaw. J.P.’s pain is described as crushing or
viselike in quality, which also is common; a fullness in the throat or jaw may occur
simultaneously or in lieu of chest pain. In some cases, the patient may not consider
these sensations as pain, describing them instead as a sense of pressure or heaviness.
Many patients complain of SOB. J.P.’s symptoms are related to exercise and exertion
—both known precipitating factors of angina. Most episodes of exertional angina last
several minutes in duration and are relieved with rest. Because J.P. has never sought
medical attention for his chest pain, his response to NTG cannot be determined.
After getting a detailed description of J.P.’s symptoms, his physician can
characterize his chest pain and make a global assessment. Initially, the chest pain
should be classified as either typical angina, atypical angina, or noncardiac chest
pain. Furthermore, angina should also be classified as either stable or unstable. This
distinction is important because it indicates whether his short-term risk of an acute
coronary event could be life-threatening. Attempts to categorize J.P.’s anginal
symptoms on an objective measurement scale (e.g., Canadian Cardiovascular Society
Grading Scale) can be misleading.
45 For example, a sedentary 65-year-old patient’s
class II symptoms may be tolerable, but the same symptoms could significantly
disable an active 50-year-old patient.
J.P.’s chest pain is of a quality and duration characteristic of angina, provoked by
exertion, and relieved by rest; therefore, J.P.’s constellation of symptoms can be
classified as typical chest pain. J.P.’s symptoms do not occur at rest; however, they
should be classified as stable angina.
CASE 12-1, QUESTION 2: Assess J.P.’s physical examination. What signs and symptoms are relevant to
The physical examination typically provides little information about the presence
of CAD. The most useful findings pertain to the cardiovascular system where heart
rate and BP can be increased during an acute anginal episode. J.P.’s physical
examination is characteristic of a man of his age with angina.
hypertensive, but his cardiac examination is normal. The presence of murmurs would
have required further workup; the absence of a third heart sound suggests that the left
ventricle may be functioning normally. (See Chapter 14, Heart Failure, for a
description of third heart sounds.) The absence of a fourth heart sound in J.P. is
indicative of a low probability of cardiac end-organ damage resulting from systemic
hypertension. His chest radiograph, which is normal, does not present evidence of
other complications commonly associated with myocardial ischemia (e.g., enlarged
J.P.’s physical examination should also evaluate the possibility of the presence of
atherosclerosis in other major vascular beds (peripheral vascular disease,
cerebrovascular disease, abdominal aortic aneurysm). The presence of xanthomas
would suggest severe hypercholesterolemia, but these were not noted in J.P.
CASE 12-1, QUESTION 3: What other objective diagnostic procedures are helpful to confirm CAD and
A 12-lead ECG indicates there is no ongoing ischemia at this time. As such, it
does not help confirm the diagnosis of CAD. An echocardiogram could be used to
better assess cardiac structure and function, including ruling out other potential
causes for myocardial ischemia such as valvular dysfunction or pericardial disease,
but would not definitively confirm the presence of CAD. Electron bean computed
tomography or CCTA could be used to detect the presence of coronary
atherosclerosis, but in J.P. would not offer vital prognostic information available
with other testing modalities.
Given J.P’s current lifestyle and activity level, he would likely be able to tolerate
exercise treadmill testing. Treadmill testing would be an appropriate initial
diagnostic modality in J.P. due to its noninvasive nature, reliability with established
protocols, as well as the ability to offer prognostic information regarding the risk of
MI and death for J.P. Therefore stress testing, in this case with exercise treadmill
versus pharmacologic means, is an excellent initial diagnostic modality to use in J.P.
procedure influence future therapy?
Coronary catheterization and angiography is the best test for the definitive
diagnosis of CAD. In addition, angiography is the most accurate means of identifying
less common causes of chronic stable angina, such as coronary artery spasm.
Although angiography is effective at identifying flow-limiting atherosclerotic
plaques in the coronary vasculature, it cannot provide information on whether those
lesions are causing clinical symptoms. Stress testing is often a more appropriate
initial modality to first characterize the myocardial ischemia that takes place with
exertion. Patients with significant ischemia via stress testing should then undergo
cardiac catheterization to determine the nature and extent of disease. The results of
angiography will be useful in determining the risk of death or MI in J.P. and,
subsequently, the course of needed treatment. For example, patients who have a
significant stenosis in the left main coronary artery are at high risk of death and
Risk Stratification and Prognosis
The prognosis of patients with stable angina is variable and dependent on the
presence of other factors and comorbid conditions. The extent of CAD, quantification
of ventricular function, the response to stress testing, as well as the initial clinical
evaluation all help to provide an estimate of risk in a given patient. Developing a
level of risk for a particular patient helps determine the appropriate treatment
J.P.’s history and physical examination suggest he does not have HF; poor LV
elevates his risk for future cardiovascular events. The absence of other major
comorbid conditions, myocardial dysfunction, along with the current extent of CAD
indicates that J.P.’s prognosis at this time is favorable provided he initiate
appropriate treatment strategies demonstrated to reduce morbidity and mortality in
Medical Management of Chronic Stable Angina
CASE 12-1, QUESTION 6: How should J.P. be managed at this time? Should he undergo revascularization
with PCI or CABG, or be managed medically?
As discussed previously, goals for managing CAD and angina in J.P. include relief
of symptoms and reduction of myocardial ischemia to improve quality of life, as well
as prevention of major complications of CAD such as acute MI and death.
Depending on the patient, both goals may be accomplished through surgical
revascularization, medical management, or both. Regardless of the treatment strategy
chosen to relieve ischemic symptoms, therapies that prevent death (vasculoprotective
agents) should receive priority.
Presently, CABG is not the best option for J.P. because the usual indications for
surgical therapy include presence of left main CAD, presence of three-vessel disease
(especially if LV function is impaired), or ineffectiveness of medical therapy.
However, revascularization with PCI is a potential option along with medical
management alone. Although PCI would offer no mortality advantage over medical
therapy at this time, it has been shown to decrease the incidence of recurrent
symptoms in the short term (1 year).
If J.P. can implement aggressive lifestyle
modifications and control of risk factors, progression of CAD and control of
ischemic symptoms will be similar to PCI within a 5-year time frame.
strategies, including the pros and cons of PCI or medical management alone, should
be offered to J.P. so that an informed decision can be made in accord with his
wishes. Overall, J.P. will probably do well with medical therapy. His life
expectancy depends on progression of the disease and development of other
complications of CHD (HF, MI, sudden cardiac death).
RISK FACTORS AND LIFESTYLE MODIFICATIONS
CASE 12-1, QUESTION 7: What independent risk factors for CAD are present in J.P.? Which of these may
The first step in the treatment of any patient with chronic stable angina or CAD
should be the modification of any existing risk factors and the adoption of a healthy
lifestyle. By addressing the underlying circumstances, which likely led to the
development of CAD, a significant impact can be made at halting the progression of
the disease and preventing complications of CAD. Current recommendations for the
goals for risk factor management are listed in Table 12-3.
risk factor goals, attention should be paid to evidence that favors specific drug
therapies that have evidence supporting reductions in morbidity and mortality.
Examples would include the use of HMG-CoA reductase inhibitors in the treatment
1,2 as well as the use of ACE inhibitors for the treatment of
J.P. has several risk factors for CAD, some of which cannot be altered, such as
middle age, male sex, and a strong family history of CAD. Risk factors, such as
hypertension, obesity, hypercholesterolemia, smoking, and possibly stress, can
potentially be modified to decrease the likelihood of adverse sequelae for J.P. His
hypertension should be controlled and statin therapy should be initiated (see Chapter
8, Dyslipidemias, Atherosclerosis, and Coronary Heart Disease). A fasting Hgb A 1c
should be drawn with a goal of less than 7% (see Chapter 53, Diabetes Mellitus).
Dietary modification and weight reduction for J.P. are mandatory, because they
positively influence several risk factors. J.P., however, does not smoke cigarettes,
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