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298 PART 3: Cardiovascular Disorders
■ ANGIOTENSIN CONVERTING ENZYME INHIBITORS Use of an IABP is indicated in unstable angina when the angina and
Angiotensin converting enzyme (ACE) generates angiotensin II from attendant ECG abnormalities are persistent and refractory to maximal
pharmacologic therapy. An IABP also may be inserted in patients who
angiotensin I and also catalyzes the breakdown of bradykinin. Thus ACE
inhibitors can decrease circulating angiotensin II levels and increase are stable and have undergone angiography but in whom precarious
coronary lesions (eg, left main coronary artery stenosis) have been
levels of bradykinin, which in turn stimulates production of nitric oxide
by endothelial nitric oxide synthase. In the vasculature, ACE inhibition identified. Typically, these patients are maintained on the device while
awaiting surgery or angioplasty.
promotes vasodilation, and tends to inhibit smooth muscle proliferation,
Although insertion of an IABP can result in immediate and dra-
platelet aggregation, and thrombosis. matic relief of myocardial ischemia, there are potential complications,
38
The major hemodynamic effect of ACE inhibition is afterload reduc-
tion, which is most important as an influence of myocardial oxygen including aortic dissection, bleeding, femoral neuropathies, renal failure
from renal artery occlusion, arterial thrombi and emboli, limb ischemia,
demand in patients with impaired left ventricular function. A recent
study, however, has demonstrated that ACE inhibition may be beneficial and line sepsis. These potential complications must be weighed in deter-
mining whether an IABP should be inserted.
to prevent recurrent events in high-risk patients. The HOPE trial of
9297 patients with documented vascular disease or atherosclerosis risk Coronary Angiography: If anginal symptoms persist despite maximal
factor showed that ramipril (target dose 10 mg/d) reduced cardiovas- medical therapy, coronary angiography with an aim toward possible
cular death, myocardial infarction (MI), and stroke by 22% compared revascularization should be considered. Frequent anginal episodes or
to placebo. Patients were normotensive at the start of the trial, and episodes that are difficult to control with conventional antianginal
28
the magnitude of benefit observed was not explained by the modest medications may suggest impending infarction. Under these circum-
reduction in blood pressure (2-3 mm Hg). The ACC/AHA guidelines stances, early angiography is indicated. In cases in which the patient
28
recommend use of ACE inhibitors in most cases as routine secondary is stabilized readily with pharmacologic agents, angiography may be
prevention for patients with known CAD, particularly in diabetics with- delayed or even deferred altogether. One must keep in mind that coro-
out severe renal disease. 29 nary angiography is not a therapeutic intervention, but a diagnostic
■ LIPID-LOWERING AGENTS test. Angiography is of little tangible value if there are no viable revas-
cularization options. The optimal timing of angiography in patients
Extensive epidemiologic, laboratory, and clinical evidence provides with non-ST elevation acute syndromes is a separate and evolving
a convincing relationship between cholesterol and coronary artery issue that will be considered in the section on NSTEMI.
disease. Total cholesterol level has been linked to the development
of CAD events with a continuous and graded relation, with a close
association with LDL cholesterol. Numerous large primary and sec- ST ELEVATION MYOCARDIAL INFARCTION
30
ondary prevention trials have shown that LDL cholesterol lowering is Symptoms suggestive of MI may be similar to those of ordinary angina
associated with a reduced risk of coronary disease events. The earli- but are usually greater in intensity and duration. Nausea, vomiting, and
est lipid-lowering trials used bile-acid sequestrants (cholestyramine), diaphoresis may be prominent features, and stupor and malaise attrib-
fibric acid derivatives (gemfibrozil and clofibrate), or niacin in addition utable to low cardiac output may occur. Compromised left ventricular
to diet, achieving a reduction in total cholesterol of 6% to 15%, accom- function may result in pulmonary edema with development of pulmo-
panied by a consistent trend toward a reduction in fatal and nonfatal nary bibasilar crackles and jugular venous distention; a fourth heart
coronary events. 31 sound can be present with small infarcts or even mild ischemia, but a
HMG-CoA reductase inhibitors (statins) produce larger reductions in third heart sound is usually indicative of more extensive damage.
cholesterol, with more impressive clinical results. Statins have been dem- Patients presenting with suspected myocardial ischemia should
onstrated to decrease the rate of adverse ischemic events and mortality undergo a rapid evaluation. A 12-lead electrocardiogram should be
when used both as primary prevention in high-risk patients, 32,33 and as performed and interpreted expeditiously. Initial therapy should include
secondary prevention in patients with documented CAD. 34-36 The goal aspirin, 160 to 325 mg orally, sublingual nitroglycerin (unless systolic
of treatment is an LDL cholesterol level less than 100 mg/dL, although pressure is <90 mm Hg), and usually oxygen, even though hard evidence
37
there appears to be a linear relationship between LDL levels and events, for benefits of oxygen in patients without hypoxia is not compelling. 40,41
and many clinicians recommend an LDL goal of <70 mg/dL, especially Opiates should be used to relieve pain, and also to reduce anxiety, the
for secondary prevention. Maximum benefit may require management salutary effects of which have been known for decades and must not
of other lipid abnormalities (elevated triglycerides, low HDL cholesterol) be underestimated. It is also important to provide reassurance to the
and treatment of other atherogenic risk factors. patient.
■ REFRACTORY ANGINA provides strong evidence of thrombotic coronary occlusion, the patient
ST-segment elevation of at least 1 mV in two or more contiguous leads
Intra-Aortic Balloon Pump Counterpulsation: When angina remains should be considered for immediate reperfusion therapy. The diagnosis
refractory to maximal medical therapy, intra-aortic balloon pump coun- of STEMI can be limited in the presence of preexisting left bundle-
terpulsation may be considered. The intra-aortic balloon pump (IABP) branch block (LBBB) or a permanent pacemaker. Nonetheless, new
is a device that is inserted via the femoral artery into the descending LBBB with a compatible clinical presentation should be treated as acute
thoracic aorta just distal to the aortic arch. A 40-mL balloon at the tip myocardial infarction and treated accordingly. Indeed, data suggest that
of the catheter is inflated in diastole by a pneumatic pump in synchrony patients with STEMI and new LBBB may stand to gain even greater
with closure of the aortic valve, and is deflated on opening of the aortic benefit from reperfusion strategies than those with ST elevation. 42
or to the arterial pressure recording. By deflating during ventricular ■ THROMBOLYTIC THERAPY
valve. Inflation and deflation are gated to the R and T waves on the ECG
systole, ventricular afterload is reduced, resulting in significant decreases Early reperfusion of an occluded coronary artery is indicated for all
in myocardial wall stress and significant decreases in myocardial oxygen eligible candidates. Overwhelming evidence from multiple clinical trials
requirements. Furthermore, inflation during diastole augments coro- demonstrates the ability of thrombolytic agents administered early in
38
nary blood flow by increasing coronary perfusion pressure. The main the course of an acute MI to reduce infarct size, preserve left ventricular
way in which an IABP relieves myocardial ischemia is by decreasing function, and reduce short-term and long-term mortality. 43,44 Patients
oxygen demand through afterload reduction. 39 treated early derive the most benefit. Indications and contraindications
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