52-Year-Old Male With Chest Tightness, Shortness of Breath, and Mild Nausea

The following case was provided by NLEC Faculty Member Michael B. Clearfield, DO, Chairman and Professor at the University of North Texas Health Science Center in Fort Worth, Texas.

AT is a 52-year-old black male who presents to the emergency room with chest tightness, shortness of breath, and mild nausea over the previous 4 hours. The patient states that the symptoms started while he was mowing the lawn but abated once he stopped, only to recur about an hour later while he was watching television. He denies any associated chest pain or diaphoresis.
   Further discussion revealed that, during the previous 3 weeks, AT had noticed a similar but less severe chest discomfort occurring once or twice a week while working in his garden. He described the discomfort as a sensation of tightness associated with mild shortness of breath, but no pain, nausea, or diaphoresis, which resolved within 5 minutes after cessation of activity. Until the day of admission to the hospital, AT's chest discomfort had not occurred at rest.
   Prior history revealed that the patient had smoked a pack of cigarettes per day for approximately 20 years; he stopped smoking 10 years ago. AT also had a history of hypertension, which was controlled on therapy.
   In the emergency room, the patient had an ECG performed, which was interpreted as no acute change with nonspecific ST- and T-wave changes. He was treated with intravenous access, supplemental oxygen, aspirin, and nitroglycerin. The chest tightness diminished following the emergency room treatment, and the patient was transferred to the telemetry unit for observation. Serial cardiac enzymes revealed a bump in both CPK-MB and troponin levels 6 hours after admission. A repeat ECG revealed 2 mm ST-segment depression in the inferior leads.
   The remainder of the patient's hospitalization was unremarkable. Metoprolol was substituted for amlodipine. Five days after admission, the patient underwent submaximal exercise test and a fasting lipid profile. The stress test revealed no symptoms or significant ECG changes.
   The patient was sent home on an American Heart Association Step I diet and the following medications: aspirin, metoprolol, lisinopril/hydrochlorothiazide.

Discussion
This patient's diagnosis is one of an ACS. The term "acute coronary syndrome" has been used to describe the spectrum of clinical conditions from unstable angina to MI. Frequently, as in this case, it is difficult to determine whether a patient has unstable angina or has experienced a non–Q-wave MI. Both unstable angina and non–Q-wave MIs may present in a similar manner that can only be distinguished by cardiac enzyme changes hours or days later. In this case, it was determined that the patient had a non–Q-wave MI of the inferior wall.
   Patients who survive an AMI have a high mortality rate associated with its recurrence. It is, therefore, imperative that treatment be focused on decreasing the chance of a recurrent event. Major factors determining a higher risk and poorer prognosis post-MI include decreased left ventricular function, recurrent ischemia, and life-threatening arrhythmia. Other factors that help determine a poor long- and short-term prognosis post-MI include advanced age, heart failure, anterior infarction, hypotension, and tachycardia.¹ The patient in this case had none of these complications, thus conferring the status of an uncomplicated MI.

Figure. Temporal trends in the receipt of aspirin, ß-blockers, and lipid-lowering medications before hospital admission for recurrent acute myocardial infarction

Worcester Heart Attack Study, 1986-1995. Adapted from McCormick D et al. Arch Intern Med. 1999;159:561-567.

   Several medications have been shown to reduce a recurrent AMI in patients who have survived an initial MI. The effectiveness of aspirin and ß-blocker therapy has been established; they comprise the cornerstone of therapy in these patients. Despite the encouraging trend of increased use of these medications (Figure), many of our patients are still not being afforded their benefits.² Recent data have indicated the benefit of angiotensin-converting enzyme (ACE)-inhibitors in the treatment of AMI, even in patients without evidence of left ventricular dysfunction or heart failure.³ As can be noted in this case, AT was given all three options to decrease his risk for a recurrent AMI.
   Another option that should have been considered in this case was more aggressive treatment of the patient's lipids during his hospitalization for the acute event. A lipid profile was not assessed on admission but was performed prior to discharge. If a patient's LDL-C is between 100 and 130 mg/dL, clinicians should decide whether to institute drug treatment by utilizing current guidelines in treating post-MI patients, weighing potential benefits vs side effects and cost, and applying their clinical judgment.⁴ As with ß-blockers and aspirin, lipid-lowering treatment in patients post-MI also leaves substantial opportunity for improvement (Figure).²
   To complicate matters further in this patient's case, the lipid profile attained on day 5 post-AMI may not be representative of baseline lipid values. Within the first 24 to 48 hours after an acute event, lipid values can significantly decrease/increase by as much as 50%, and the effect can last up to 3 months.^5,6 Thus, without knowledge of baseline lipid values, the utility of post-MI lipid values relative to the guidelines is suspect.
   The 4S,⁷ the CARE trial,⁸ and the LIPID trial⁹ have demonstrated that treatment with HMG-CoA reductase inhibitors (statins) reduces mortality if initiated 3 to 6 months after an AMI. (These studies specifically did not include patients within the first 3 months of an AMI.)
   The issue of acute treatment of lipids during the first days to weeks after an AMI is more controversial. In a review of a large prospective cohort from Sweden, early statin treatment initiated before or at the time of hospital discharge following AMI reduced 1-year mortality by 25%.¹⁰ Results are awaited in the MIRACL trial. In this study, patients were randomized to either placebo or atorvastatin (80 mg) 24 to 96 hours after admission for unstable angina or non–Q-wave MI.¹¹ Patients qualified for randomization into the study if their TC was 270 mg/dL (310 mg/dL at sites in Poland and South Africa); there was no lower TC limit. Although the results have been presented at scientific meetings, they await publication.

Comment
AT would meet the criteria for inclusion into the MIRACL trial. Aggressive lipid-lowering treatment during the acute phase of his non–Q-wave MI should be of value in reducing his risk for recurrent ischemic events. This type of therapy should be considered along with the other proven modalities (such as ß-blockade, aspirin, and, possibly, ACE-inhibition) in the treatment of acute coronary syndromes.

References