EPIDEMIOLOGIC TRENDS, INFLUENCE OF AGING
The prevalence of acquired cardiovascular disease in society,
its social and economic implications, and the temporal changes over the last 2 decades
have been well documented.[1]
Profound advances
in our understanding of the basic biologic mechanisms underlying cardiovascular disease
and thus the potential to examine these mechanisms, as well as rapid technologic
advances (e.g., drug-eluting stents, nonsurgical valve replacement[2]
),
suggest that the number of patients presenting for cardiac surgery could continue
to decline. Certainly, the most recent data for surgical revascularization procedures
would substantiate this conclusion. However, interventions such as stents, similar
to surgical revascularization, fail to address the fundamental underlying problem
and in many cases may merely defer rather than subvert the need for surgery. Moreover,
the increasing armamentarium of primary preventive measures (more effective treatment
of dyslipidemias, angiotensin-converting enzyme [ACE] inhibitors, which have benefits
beyond their anti-hypertensive effects[3]
) is not
readily disseminated to the population at large. Even if more successfully adopted,
primary interventions are likely to merely postpone disease evolution, albeit in
a relatively disease-free state. Thus, the well-established common risk factors
for acquired cardiovascular disease (hypertension, cigarette use, hyperlipidemia,
diabetes, obesity) are most likely to continue to exert a profound influence on the
epidemiology of acquired cardiovascular disease. The age-adjusted death rates from
1986 to 1996 support this overall conclusion.[1]
Although the fundamental molecular and genetic basis of aging is increasingly being
understood,[4]
[5]
[6]
we can only modify the rate at which it occurs.
Taken together, the patient population presenting for various cardiac surgical procedures
will probably remain robust to a degree that will sustain cardiovascular anesthesia
as a subspecialty. Going forward, patients being evaluated for surgery are likely
to be older, undergo repeat surgical procedures, and have more comorbid conditions.
It is increasingly recognized that age, even in the absence of
vascular disease, is itself associated with changes in both the vascular tree and
the myocardium and may be an independent risk factor for cardiovascular events ( Fig.
50-1
) (also see Chapter 62
).
[7]
In the absence of disease, baseline parameters
of cardiovascular function are relatively similar to those measured in younger controls
and include left ventricular end-diastolic volume, left ventricular end-systolic
volume, ejection fraction,[8]
response to β-adrenergic
blockade,[9]
coronary reserve,[10]
and vascular smooth muscle relaxation.[11]
However,
endothelial
Figure 50-1
Changes in the vasculature and heart with aging in health
may also be construed as risk factors for cardiovascular disease leading to heart
and brain disorders in older age. LV, left ventricular. (Redrawn from Lakatta
E: Aging effects on the vasculature in health: Risk factors for cardiovascular
disease. Am J Geriatr Cardiol 3:11–17, 1994.)
dysfunction and impaired nitric oxide (NO) release are important features of aging
vessels[12]
and contribute to an impaired arteriolar
vasodilator response, increased vascular stiffness, and left ventricular myocardial
changes (modest left ventricular hypertrophy and prolonged relaxation) induced by
vascular-ventricular coupling. Indeed, it is increasingly being recognized that
systolic blood pressure and pulse pressure may be better barometers of arterial stiffness
and of the amplitude and timing of wave reflections than diastolic blood pressure
is and thus a more informative cardiovascular risk factor.[13]
Impaired sympathetic modulation of the cardiovascular system is also a central feature
of aging. In aging, although gross functional parameters of cardiac performance
appear normal at rest, the response to exercise is markedly impaired, and exercise
unmasks limited cardiovascular reserve, as indicated by an impaired heart rate response,
impaired inotropic response, and a decrease in maximum work capacity and oxygen consumption.
Moreover, cellular and molecular studies in animal models of aging clearly demonstrate
age-related changes in excitation, calcium cycling, myofilament contraction, and
gene expression ( Table 50-1
).
Exercise unmasks the lack of cardiovascular reserve in aging. Perioperative stress
could be viewed as analogous to exercise and may partly explain why patients with
relatively normal baseline test results do not necessarily have an event-free perioperative
journey.
