A 52-year-old Caucasian man presents for an annual physical examinaion. He complains of fatigue and daytime sleepiness. He has a sedentary job and a long daily commute. He eats fast food once a day. He drinks 2 to 3 bottles of beer most nights. His past medical history is significant for essential hypertension and hypercholesterolemia. His medications include lisinopril 10 mg daily, hydrochlorothiazide 25 mg daily, and atorvastatin 40 mg daily. His cardiovascular review of systems is negative.
His body mass index is 33. He has a pulse rate of 82 and a seated blood pressure of 148/92 mm Hg. Neck size is 18 inches. His cardiac and pulmonary examinations are normal and he has no pitting edema in the lower extremities.
What lifestyle modification issues should be discussed?
What additional diagnostic information is needed?
Are changes to his medications indicated at this time?
Hypertension (HTN) is defined as systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg. Hypertensive heart disease is the response of the heart to elevated arterial pressure and peripheral vascular resistance. There is an increase in afterload on the left ventricle. There are several cardiac manifestations of this, including left ventricular hypertrophy (LVH), cardiac dysrhythmias, ischemic heart disease, and congestive heart failure (CHF).
The prevalence of HTN in the United States is estimated to be 29%. The prevalence among Americans older than age 60 years is 65%. HTN is more common in non-Hispanic black adults, who are 40% to 50% more likely to have HTN. There is no difference in prevalence between women and men. The rate of control of diagnosed HTN in the United States has been improving. The rate of control was 31.5% in the year 2000 and is now 54%. The Healthy People 2020 target is 61.2% controlled by the year 2020.1
Resistant HTN is defined as a blood pressure above goal in spite of concurrent use of 3 antihypertensive medications of different classes. One of those medications should be a diuretic, and all should be at optimal doses. If a patient’s blood pressure is controlled on 4 or more medications, then that patient is still considered to have treatment-resistant HTN. Some patient factors associated with resistant HTN are older age, obesity, excessive dietary sodium intake, chronic kidney disease, diabetes mellitus, black race, and female sex.
Blood pressure is a function of cardiac output and peripheral resistance. An increasing cardiac output or an increase in peripheral resistance will lead to an increase in blood pressure. The pathogenesis of essential HTN is multifactorial and complex. Excessive dietary sodium or renal sodium retention results in increased intravascular fluid volume and elevated blood pressure. An increase in sympathetic nervous system activity will increase cardiac output and by that mechanism increase blood pressure. Activation of the renin angiotensin system would be expected to cause an increase in peripheral resistance and therefore increase blood pressure. Obesity, hyperinsulinemia, and endothelial factors can also lead to increased peripheral resistance and therefore increase blood pressure. More than 20 gene polymorphisms have been reported in HTN.
In the clinical evaluation of HTN, there are several important things to consider. Adherence to prescribed medications must be reviewed with each patient. Failure to take medications as prescribed is the most common cause of poorly controlled HTN. Furthermore, medications prescribed for other conditions might increase blood pressure.
The possibility of white-coat HTN must also be considered. Blood pressure measurements obtained at home at various times of day should be requested and then compared to office blood pressures. Lifestyle factors are also important. Dietary factors such as excessive sodium intake and excessive alcohol intake may increase blood pressure. Lack of physical activity and obesity may also increase blood pressure.
In approximately 10% of patients with HTN, there is a secondary cause. If HTN is sudden in onset, occurs at a young age, is associated with hypokalemia, or is treatment-resistant, then secondary causes should be considered.
Hypertensive heart disease refers to a variety of abnormalities ranging from asymptomatic LVH to systolic dysfunction to diastolic dysfunction to arrhythmias. In the setting of chronically elevated blood pressure, the left ventricular wall may thicken or dilate in order to minimize wall stress. Ultimately clinical heart failure (HF) develops with either preserved or reduced left ventricular ejection fraction. When there is wall thickening, the LVH is classified concentric. When there is chamber dilation but no increase in wall thickness, the LVH is eccentric. The response of the left ventricle to high blood pressure varies among individuals. Black patients with HTN have greater risk for LVH and concentric geometry than white patients (Figure 3-1).2
LVH is associated with microvascular disease, which results in reduced coronary blood flow and increased myocardial oxygen demand. In addition, HTN leads to acceleration of atherosclerotic coronary artery disease (Figure 3-2). Plaque rupture is more common in patients who have LVH.3
Normal blood pressure is <120/80 mm Hg. Stage 1 HTN is defined by blood pressure of 142 to 159/90 to 99 mm Hg. Stage 2 HTN is ≥160 over ≥100. Hypertensive crisis is defined by a blood pressure >180/>110 mm Hg.
For office measurement of blood pressure, the patient should be seated quietly for 5 minutes with the arm bare and supported at the level of the heart. The blood pressure cuff should circle at least 80% of the circumference of the arm. Blood pressure should be measured in both arms. Three sets of readings at least 1 week apart should be obtained to make a diagnosis of HTN.
Automated office blood pressure measurement has been demonstrated to reduce the white-coat response. Automated office blood pressure is also superior to manual office blood pressures in terms of correlation with ambulatory blood pressure monitoring.4
There is a normal decrease or “dip” in blood pressure at night related to sleep and decrease in physical activity. A patient who does not have this decrease is a “nondipper.” Several studies have shown that nondippers have worse cardiovascular outcomes including strokes, cardiac hypertrophy, diastolic dysfunction, and arrhythmias. A typical nocturnal decrease in blood pressure is 15%.
White-coat HTN is defined as a blood pressure measured by a physician or nurse persistently ≥140 mm Hg systolic or ≥90 mm Hg diastolic when out-of-office blood pressure is <130 systolic and <80 diastolic for 24-hour blood pressure and <135/85 mm Hg for a home blood pressure. The estimated prevalence of white-coat HTN is 30% to 40% of the population with an elevated office blood pressure.
Masked HTN is a condition in which clinic blood pressure is below 140/90 mm Hg, but home blood pressure or 24-hour blood pressure is above normal. Available data indicate that 10% of the general population has masked HTN. The cardiovascular risk associated with masked HTN is nearly the same as the risk with true HTN.
Ambulatory blood pressure monitoring is better than conventional office-based blood pressure measurement in the prediction of cardiovascular outcomes. This was demonstrated in a prospective study published in 1983 by Perloff and later confirmed by other investigators. Blood pressures at night and ambulatory systolic blood pressures have been the strongest predictors for cardiac death. The use of a 24-hour ambulatory blood pressure monitor for all patients with HTN is limited due to the cost and convenience for the patient. Self-monitoring of blood pressure may be used in order to identify a subset of patients who would benefit from wearing a 24-hour monitor. If there is a large disparity between clinic and home measurements, then a formal 24-hour assessment might be helpful. Measurement of home blood pressures twice daily in the morning and evening for 1 to 2 weeks is a simple and low-cost method.
