MICHEL E. SAFAR and MICHAEL F. O'ROURKE One of the principal problems of hypertension is the precise definition of blood pressure as a cardiovascular risk factor. Clinicians indicate peak systolic pressure and end diastolic pressure in the brachial artery as the principal criteria for blood pressure measurement. Consequently, these values are as indicators for clinical management and therapeutic adjustment. This used methodology, based on indirect blood pressure measurements at the site of the brachial artery relates only to the highest and lowest pressure in that vessel, and does not give any information of the blood pressure curve itself; this carries more information than peak systolic pressure and end diastolic pressure. As a first step in better analysis of the blood pressure curve, research workers in experimental hypertension defined in addition to peak systolic pressure and end diastolic, another blood pressure value, mean arterial pressure, i. e. the average pressure throughout the cardiac cycle, and about which pressure fluctuates. This is the pressure recorded by Hales [1] and by Poiseuille [2] in their pioneering studies. By application of Poiseuille's Law, this definition of mean arterial pressure led to the concept that increased mean arterial pressure (and therefore hypertension) was related, at any given value of cardiac output, to an increase in vascular resistance, i. e. to a reduc tion in the caliber of the small arteries.

The hemodynamic mechanisms of hypertension are often limited to the study of three dominant parameters: blood pressure, cardiac output and vascular resis tance. Accordingly, the development of hypertension is usually analyzed in terms of a 'struggle' between cardiac output and vascular resistance, resulting in the classical pattern of normal cardiac output and increased vascular resistance, thus indicating a reduction in the caliber of small arteries. However, during the past years, the clinical management of hypertension has largely modified these simple views. While an adequate control of blood pressure may be obtained with antihypertensive drugs, arterial complications may occur, involving mainly the coronary circulation and suggesting that several parts of the cardiovascular system are altered in hypertension. Indeed, disturbances in the arterial and the venous system had already been noticed in animal hypertension. The basic assumption in this book is that the overall cardiovascular system is involved in the mechanisms of the elevated blood pressure in patients with hypertension: not only the heart and small arteries, but also the large arteries and the venous system. For that reason, the following points are emphasized. First, the cardiovascular system in hypertension must be studied not only in terms of steady flow but also by taking into account the pulsatile components of the heart and the arterial systems. Second, arterial and venous compliances are altered in hypertension and probably reflect intrinsic alterations of the vascular wall."

Hypertension is the major cause of left ventricular hypertrophy. While the electrocardiogram is an extremely insensitive measure of anatomic left ven- tricular hypertrophy, it provides a time-tested important marker of an adverse cardiovascular outcome. There has been a recent temporal decrease in the incidence of electrocardiographic evidence of L VH even within the hyperten- sive population; no doubt this is the result of large antihypertensive treatment experts. Anatomical evidence of left ventricular hypertrophy is best docu- mented pre-morbidly using echocardiographic techniques. It therefore ap- pears that between 20 and 50 percent of the hypertensive population has left ventricular hypertrophy by echo cardiographic techniques. The prognostic significance of the echocardiographically determined increase in left ventric- ular mass is just beginning to be evaluated. Early information suggests that there is an increased rate of cardi~)Vascular morbidity in patients with echo car- diographic evidence of increased left ventricular mass. However, this in- formation is only preliminary, and as yet only a limited number of events have been reported. Far more supporting information will be required before the full impact of echocardiographically-detected left ventricular hypertrophy can be determined. Nevertheless, it must be stated that the electrocardiogram still has the greatest predictive value of cardiovascular morbid and mortal events when the pattern of left ventricular hypertrophy plus repolarization abnormal- ities are present.

The hemodynamic mechanisms of hypertension are often limited to the study of three dominant parameters: blood pressure, cardiac output and vascular resis­ tance. Accordingly, the development of hypertension is usually analyzed in terms of a 'struggle' between cardiac output and vascular resistance, resulting in the classical pattern of normal cardiac output and increased vascular resistance, thus indicating a reduction in the caliber of small arteries. However, during the past years, the clinical management of hypertension has largely modified these simple views. While an adequate control of blood pressure may be obtained with antihypertensive drugs, arterial complications may occur, involving mainly the coronary circulation and suggesting that several parts of the cardiovascular system are altered in hypertension. Indeed, disturbances in the arterial and the venous system had already been noticed in animal hypertension. The basic assumption in this book is that the overall cardiovascular system is involved in the mechanisms of the elevated blood pressure in patients with hypertension: not only the heart and small arteries, but also the large arteries and the venous system. For that reason, the following points are emphasized. First, the cardiovascular system in hypertension must be studied not only in terms of steady flow but also by taking into account the pulsatile components of the heart and the arterial systems. Second, arterial and venous compliances are altered in hypertension and probably reflect intrinsic alterations of the vascular wall.