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Improving our insights into the genetic predisposition to
cardiovascular disease is one of the most important challenges in
our field in the next millennium, not only to unravel the cause of
disease but also to improve the selection of patients for
particular treatments. Nowadays, for example, subjects with a
cholesterol above a particular plasma level are exposed to a
cholesterol lowering regime based upon the beneficial outcome of
epidemiological studies which include subjects not prone to the
disease, despite a plasma cholesterol above the accepted level.
Identification of the patients who are genetically predisposed to
the consequences of this disorder will reduce the number of
subjects unnecessarily treated and, hence, the costs of health
care. Because in most cardiovascular diseases the genetic component
is a consequence of more than one gene defect, only limited
progress has as yet been made in identifying subjects genetically
at risk. For example, in hypertension only in less than 10% of the
patients the genetic defect has been identified. It has been known
for quite some time that in heart and blood vessels fetal genes are
as high blood pressure and upregulated or induced when they are
exposed to such disorders ischemia. Little is known about the
function of these genes in the cardiac and vascular adaptation to
these disorders; only guesses can be made.
Advances in cellular physiology and molecular biology have now
disclosed the metabolic changes and adaptational responses of the
heart to various kinds of stresses. Topics covered in this volume
include the regulation of myocardial proteins in mechanical
overload, the alteration of adrenoceptors in the stressed heart,
metabolic adaptation in cardiac hypertrophy, intracellular calcium
metabolism in the ischemia-reperfused myocardium, calcium overload
as a cause of myocardial stunning, acquisition of ischemic
tolerance by ischemic preconditioning, factors that accelerate
myocardial injury, and ventricular remodeling in the ischemic
heart. As an update of the latest findings in basic cardiology,
this book will benefit both researchers and clinical practitioners.
Advances in cellular physiology and molecular biology have now
disclosed the metabolic changes and adaptational responses of the
heart to various kinds of stresses. Topics covered in this volume
include the regulation of myocardial proteins in mechanical
overload, the alteration of adrenoceptors in the stressed heart,
metabolic adaptation in cardiac hypertrophy, intracellular calcium
metabolism in the ischemia-reperfused myocardium, calcium overload
as a cause of myocardial stunning, acquisition of ischemic
tolerance by ischemic preconditioning, factors that accelerate
myocardial injury, and ventricular remodeling in the ischemic
heart. As an update of the latest findings in basic cardiology,
this book will benefit both researchers and clinical practitioners.
Improving our insights into the genetic predisposition to
cardiovascular disease is one of the most important challenges in
our field in the next millennium, not only to unravel the cause of
disease but also to improve the selection of patients for
particular treatments. Nowadays, for example, subjects with a
cholesterol above a particular plasma level are exposed to a
cholesterol lowering regime based upon the beneficial outcome of
epidemiological studies which include subjects not prone to the
disease, despite a plasma cholesterol above the accepted level.
Identification of the patients who are genetically predisposed to
the consequences of this disorder will reduce the number of
subjects unnecessarily treated and, hence, the costs of health
care. Because in most cardiovascular diseases the genetic component
is a consequence of more than one gene defect, only limited
progress has as yet been made in identifying subjects genetically
at risk. For example, in hypertension only in less than 10% of the
patients the genetic defect has been identified. It has been known
for quite some time that in heart and blood vessels fetal genes are
as high blood pressure and upregulated or induced when they are
exposed to such disorders ischemia. Little is known about the
function of these genes in the cardiac and vascular adaptation to
these disorders; only guesses can be made.
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