Clinical Briefs
Oral Cefpodoxime and Parenteral Ceftriaxone in Hospitalized Adults with CAP
Hospitalized patients with community-acquired pneumonia (CAP) are most often treated with parenteral antibiotics, usually with a switch to oral formulations when the clinical course is stabilized. This double-blind study compared oral cefpodoxime proxetil (Vantin) with ceftriaxone (Rocephin) in adult patients admitted for CAP (n = 88).
CAP was defined by the following criteria: 1) lung infiltrate on CXR; 2) purulent sputum with more than 25 WBCs/hpf. The study group was highly selected in that they must not have leukopenia, neutropenia, renal impairment, hepatic dysfunction, ARDS, CHF, pulmonary infarction, HIV, neoplasia requiring treatment, respiratory failure, or concomitant systemic antimicrobial therapy. Pregnant women, nursing women, and women without adequate contraception were excluded from the trial. End-of-treatment bacteriologic and clinical response were the efficacy variables.
In the cefpodoxime group, 60.6% of patients were cured (vs 57.7% ceftriaxone); 24.2% were improved (vs 23.1% ceftriaxone), and 15.2% were failures (vs 19.2% ceftriaxone). The only adverse effect difference between the therapies was that six ceftriaxone recipients developed drug-related diarrhea; none of the cefpodoxime group sustained this adversity. Bittner and associates conclude that oral cefpodoxime is equally efficacious as ceftriaxone in the treatment of CAP.
Bittner MJ, et al. JCOM 1999;6(3): 38-45.
The Association of Chronic Cough with the Risk of MI
Some recent studies have noted an association between nontraditional cardiac risk factors and cardiovascular disease. Included among these are chronic bronchitis, bacterial, and viral infections (e.g., Chlamydia, Helicobacter, cytomegalovirus). The relationship between cough and cardiovascular disease has been incompletely evaluated. Studies that associate chronic bronchitis and cardiovascular disease have omitted important potential confounders such as hampered lung function.
The Framingham heart study began in 1948 with a cohort of 5209 men and women between the ages of 28-62 who agreed to have follow-up visits every two years. A questionnaire was included, which asked about chronic cough (lasting at least 3 months of the previous year), and if chronic cough was present, was it productive or not productive.
As anticipated, chronic cough was more prevalent in smokers and men. Persons with chronic cough, whether productive or nonproductive, had a 1.9-2.1 odds ratio for MI. Since cough could represent a symptom induced by heart failure, multivariate analysis adjusted for this, without change in odds ratio. For risk of MI, in the fully adjusted multivariate analysis, persons with either productive or nonproductive chronic cough had odds ratios 1.6-1.8. Fibrinogen levels were higher in persons with chronic productive cough; it is known that persistent infection, inflammation, and cigarette smoking are all associated with increased levels of fibrinogen. It remains undetermined whether the association between cough and coronary disease is causal.
Haider AW, et al. Am J Med 1999; 106:279-284.
Isolated Clinic Hypertension is not an Innocent Phenomenon: Effect on the Carotid Artery Structure
Isolated clinic hypertension (ICH), alternatively called by such names as "white coat hypertension," presents a clinical dilemma to clinicians, since no large-scale, long-term, randomized controlled trials have examined this specific subset of patients. Zakopoulos and colleagues defined ICH as a combination of clinic blood pressure of more than 160/90 accompanied by a normal blood pressure by 24-hour ambulatory monitoring. In their group of 63 patients, they compared patients with sustained hypertension (both clinic and ambulatory blood pressure elevated) to ICH patients and normotensive individuals. The marker they chose to compare was the intimal medial thickness of the carotid artery, as determined by ultrasound, noting that this measurement has been correlated with coronary artery disease, MI, and cerebrovascular disease.
Carotid thickening was significantly more common among patients with sustained hypertension than normotensives, but the ICH group was not statistically significantly less likely to suffer such thickening.
Zakopoulos et al conclude that ICH may not be a benign finding.
Zakopoulos N, et al. Am J Hypertens 1999;12:245-250.
Clinical Scenario: The ECG shown in the Figure was obtained from a completely asymptomatic 56-year-old man. How would you interpret this ECG? What would you suspect the patient to have (have had)?
Interpretation: There is a normal sinus rhythm at a rate of 85 beats/minute. The PR interval is normal. However, everything else on this tracing is distinctly abnormal. The QRS complex is clearly prolonged in a pattern consistent with bifascicular block. Specifically, the qR complex in lead V1 with tall R wave and the wide terminal S waves in leads I and V6 are consistent with right bundle branch block (RBBB). In addition, the markedly deepened S wave component of the QRS complex in lead I, together with relatively positive complexes in the inferior leads, is consistent with the rightward axis of left posterior hemiblock (LPHB). The relatively tall and peaked P waves in lead II, and biphasic P wave in lead V1 with peaked initial component and deep negative terminal component are consistent with biatrial enlargement. Small but definite Q waves are seen both in inferior and anterior precordial leads (the latter most likely responsible for loss of the rsR’ pattern in lead V1). Finally, ST segment and T wave morphology is abnormal: The upright T wave in lead V1 suggests a primary T wave change (the T wave in lead V1 with RBBB is usually directed opposite to the tall terminal R wave)—and beginning T wave inversion in leads V3 and V5 suggests an ischemic process.
In view of the fact that this patient is completely asymptomatic, the changes on this ECG are probably not acute. However, biatrial enlargement, bifascicular block, inferior and anterior Q waves, and abnormal ST-T wave changes all strongly suggest a cardiomyopathy that is most likely ischemic in etiology from prior silent infarction(s). At the least, further evaluation with an echocardiogram would seem warranted.
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