Clinical scientists devote much of their time and effort to making precise physiologic and biologic measurements. As clinical practitioners, however, we frequently abandon the techniques learned in early medical school years as soon as we graduate. We no longer measure the height of the jugular venous pressure above an anatomic landmark (eg, the sternal angle), but rather say, “There is no JVD” (whatever that means?). The apex impulse of the heart is no longer precisely located, but the record states that there is no cardiomegaly. The heart sounds are described as S1 to S2 (that is the full description). Cardiologists often take pride in the ability to judge the severity of a stenotic lesion seen on an angiogram by “eyeballing” the study (no need for a caliper!) or in predicting the left ventricular ejection fraction or left ventricular mass by simply observing contraction on an echocardiogram without making precise measurements. And, most regrettably for those taking care of patients with hypertension, the precise measurement of blood pressure is often given short shrift in the office. For many, it is as if graduating from medical school loosens the bonds of having to be precise and quantitative.
REGRESSION OF LEFT VENTRICULAR HYPERTROPHY AND INCIDENCE OF ATRIAL FIBRILLATION
I was reminded of the need for precise measurement and quantitation of clinical data by a report from the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial.1 The LIFE trial, conducted from 1995 to 2001, was a randomized, double-blind, parallel-group study comparing an angiotensin receptor blocker (losartan-based) regimen with a β-blocker (atenolol-based) regimen on cardiovascular outcomes. In the original report there was a 33% reduction of atrial fibrillation in the losartan-treated group. It was suggested that left ventricular hypertrophy (LVH) regression might be responsible for the reduction in atrial fibrillation.
Accordingly, in the report by Okin and colleagues, 2 the LIFE study data were analyzed to determine whether in-treatment regression or continued absence of electrocardiographic (ECG) LVH during antihypertensive therapy was associated with a decreased incidence of atrial fibrillation, independent of blood pressure and specific treatment. The analysis was carried out on data from 8831 men and women with hypertension (defined as a blood pressure >140/90 mm Hg), aged 55 to 80 years, with ECG LVH by Cornell voltage-duration product or Sokolow-Lyon voltage, with no history of atrial fibrillation and without atrial fibrillation on the baseline electrocardiogram. These data demonstrated that lower Cornell product ECG LVH during antihypertensive therapy is associated with a lower likelihood of new-onset atrial fibrillation, independent of blood pressure lowering or treatment in essential hypertension. The authors suggested that antihypertensive therapy targeted at regression or prevention of ECG LVH may reduce the incidence of new-onset atrial fibrillation.
It is not surprising that these data were independent of blood pressure measured in the brachial artery since it is known that central aortic pressure, a major determinant of LVH, is lowered by losartan, but not by atenolol, despite similar levels of blood pressure measured in the brachial artery.3 This latter finding emphasizes the importance of reflected waves in determining central aortic pressure.4
Data such as these, however, remind us that precise measurements and quantitation of clinical conditions such as LVH, either by ECG or echocardiographic criteria, are necessary if we are to obtain the best results of therapy. Too often in practice, echocardiographic reports do not include quantitation of results. Clearly, this does not provide the clinician with data on which to adjust patient therapy.
MINDING P'S AND Q'S IN THE OFFICE
It is difficult to know where you are going if you do not know where you have been—Old Saw
If there is no regression of LVH following treatment of hypertension, there would certainly be reason to reassess the patient's therapy and question whether adequate control of BP was occurring throughout the day and night. To know whether regression is occurring, hypertrophy should be quantitated, either by ECG or echocardiography. The LIFE investigators utilized the Cornell voltage system.2 We have used the Romhilt Estes criteria for quantification of ECG LVH in a similar fashion. 5 Others may have other preferences.
WHAT SHOULD WE DO?
The measurement of blood pressure, heart rate, retinal changes, and evidence of LVH should be measured with the precision that we demand for blood lipids or urinary protein. These are valuable clinical data that should be quantitated for devising treatment strategies. We should insist that reports of imaging data contain precise and quantitative measurements where possible. We should record our own physical findings and personal evaluations of physiologic data (eg, the ECG), using quantitative techniques. Then, these data should be assessed over time by constructing either a flowchart or other device so that the influence of the disease and its therapy can be evaluated. If we are to treat the disease, hypertension, then we must monitor more than the course of office measurement of blood pressure. A national system of electronic medical records would facilitate this process.
Finally, we should insist that medical students and house officers hone their physical diagnostic skills and to record physical findings in precise and quantitative terms. Without these skills, they are unable to take issue with spurious data provided them by a technocrat. A reevaluation of medical school curricula may reveal that more time spent in basic science laboratories and in studying physical examination would be of more benefit to a freshman or sophomore medical student than riding an ambulance or observing patients in an emergency room (this is more relevant?). And, we should remind our students to “mind their P's and Q's.”