B. b-Adrenergic receptor antagonists 1. Mechanism of action 
 a.

b-Adrenergic
receptor antagonists inhibit the reflex tachycardia produced by nitrates. b.
Myocardial oxygen requirements are reduced due to decreases in: 
 (1) Heart
rate
 (2) Myocardial contractility (3) Blood pressure 
 2. Uses
 a. Angina (in
combination with other drugs, such as nitrates) 
 


C. Calcium channel blockers

1. Mechanism of action
 a. Block calcium movement into cells, inhibiting

excitation-contraction coupling in 
 myocardial and smooth muscle cells b.
Reduced: 
 (1) Heart rate
 (2) Blood pressure (3) Contractility 


2. Uses
 a. Ischemic coronary artery disease 
 b. Prinzmetal’s or variant

angina
 c. Also, used to treat hypertension and arrhythmias 


3. Adverse effects a. Flushing 
 b. Edema
 c. Dizziness 
 d. Constipation 


D. Metabolic Modulator 
 • Ranolazine

1. Mechanism of action 
 a. Ranolazine was first reported as a pFOX inhibitor

b. Inhibits fatty acid oxidation shifting myocardial metabolism to glucose 


c. Leads to more efficient production of ATP in ischemic tissue 


d. Now believed to inhibit the late phase of the inward sodium channel (late
INa) in 
 ischemic cells during cardiac repolarization reducing
intracellular sodium concentrations; this leads to:
 (1) Reduced
calcium influx via Naþ/Ca2þ exchange
 (2) Decreased intracellular
calcium 
 (3) Reduced ventricular tension and myocardial oxygen
consumption 


2. Use 
 • Treatment of refractory chronic angina in combination with amlodipine,

 beta blockers, or nitrates 


E. Therapeutic summary of selected drugs used to treat angina: 


III. Drugs That Affect Cholesterol and Lipid Metabolism

A. General considerations

1. Hyperlipidemia is defined as high levels of serum lipids.
 a. Primary hyperlipidemia is

caused by genetic predisposition.

b. Secondary hyperlipidemia arises as a complication of disease states, such as: (1)

Diabetes
 (2) Hypothyroidism
 (3) Cushing’s disease

(4) Acromegaly

2. Atherosclerosis may result from the following contributing factors: 
 a. High levels of
plasma lipids (particularly low density lipoprotein) b. Metabolic syndrome
(hyperinsulinemia) 
 c. Inflammation 


3. Therapy 
 a. First-line treatment
 • Control by diet and lifestyle modifications 
 b.

Second-line treatment
 • Pharmacologic intervention (Box 14-2; Table 14-2) 
 c.
The metabolism of lipoproteins and the mechanism of action of some
antihyperlipidemic drugs are summarized in Fig. 14-2. 


Beta blockers reduce heart rate and blood pressure, leading to relief of angina and improved exercise tolerance
in patients with severe angina.

Beta blockers are not effective in treating Prinzmetal’s angina.

Calcium channel blockers are effective in the treatment of Prinzmetal’s angina.

pFOX inhibitor: inhibits fatty acid oxidation; shifts metabolism to glucose for energy.