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All physicians practicing medicine encounter patients suffering
from cardiovascular disease. This book has been outlined in such a
way that vascular surgeons, general internists, neurologists and
cardiologists should be able to use it. The book covers the
complete scope of cardiac diseases in addition to chapters on
hypertension and atherosclerosis. In many patients there is a
family history of cerebrovascular accidents, myocardial infarction
or peripheral arterial disease. Also in patients reporting collaps,
palpitations and arrhythmias the family is crucial and can provide
clues to a genetic cause of the disease. This book is published to
guide physicians in the process of determining whether a genetic
component is likely to be present. Furthermore, information is
provided what the possibilities and limitations of DNA diagnostic
techniques are. Finally, the importance of newly identified
categories of potential patients, i. e. gene carriers without
symptoms or any inducible sign of disease, is highlighted. For some
patients a genetic diagnosis is essential to determine appropriate
therapy and for counseling? In some other diseases DNA diagnostic
tools are available but the relevant for the patients may be less
clear. In other families the search for a disease causing gene is
ongoing and the possibilities to find genes and to unravel the
pathophysiology of the disease is limited by the lack of patients.
To give insight into the current state of genetic diagnostics, the
authors have classified the cardiovascular diseases.
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.
Four years ago-in December 1997-the first European Science
Foundation Workshop on Cardiovascular Specific Gene Expression was
held in Maastricht. It was hardly possible to imagine the progress
in the field in those four years. In 1997, gene expression was
still an art focused on individual genes; in 200 I, many labs have
access to micro-array facilities to determine the expression of
thousands of genes simultaneously. In 1997, gene expression was an
area of fundamental research in basis molecular biology
laboratories; in 200 I, clinical cardiovascular research has
incorporated gene expression approaches. In 1997, the
interpretation of a gene expression experiment was usually
straightforward; in 200 I, advanced bioinformatics tools are needed
to approach the extreme complexities of genetic control of cell and
tissue function. The second symposium in this series is focused on
Cardiovascular Genomics. New Pathophysiological Concepts. The
organizing committee chose to invite a group of renown scientists
and young investigators around four topics of eminent importance in
cardiovascular research. These topics reflect the major present-day
clinical cardiovascular problems: atherosclerosis, hypertension,
arrhythmias and heart failure. In addition to these four
disease-driven topics, the workshop has sessions on gene expression
methodologies and cellular transplant approaches to cardiovascular
disease.
The electrocardiogram (ECG) remains the most accessible and
inexpensive diagnostic tool to evaluate the patient presenting with
symptoms suggestive of acute myocardial ischemia. It plays a
crucial role in decision making about the aggressiveness of therapy
especially in relation to reperfusion therapy, because such therapy
has resulted in a considerable reduction in mortality from acute
myocardial infarction. Several factors play a role in the amount of
myocardial tissue that can be salvaged by reperfusion therapy, such
as the time interval between onset of coronary occlusion and
reperfusion, site and size of the jeopardized area, type of
reperfusion attempt (thrombolytic agent or an intracoronary
catheter intervention), presence or absence of risk factors for
thrombolytic agents, etc. Most important in decision making on
reperfusion therapy and the type of intervention is to look for
markers indicating a higher mortality rate from myocardial
infarction. The ECG is a reliable, inexpensive, non-invasive
instrument to obtain that information. Recently it has become clear
that both in anterior and inferior myocardial infarction, the ECG
frequently allows not only to identify the infarct related coronary
artery, but also the site of occlusion in that artery and therefore
the size of the jeopardized area. Obviously, the more proximal the
occlusion, the larger the area at risk and the more aggressive the
reperfusion attempt.
The first invasive evaluation of cardiac arrhythmias in humans was
performed in 1967 in Paris (Prof. P. Coumel) and Amsterdam (Prof.
D. Durrer). This was the start of a rapid increase in our knowledge
of the diagnosis, mechanism and treatment of cardiac arrhythmias.
In that same year Prof. Hein J.J. Wellens became cardiologist in
the Wilhelmina Gasthuis in Amsterdam. Initially in Amsterdam
(1967-1977) and later on in Maastricht (from 1977), he was the
driving force for many breakthroughs in clinical cardiac
electrophysiology. With an active interplay between the knowledge
derived from the 12-lead electrocardiogram and the recordings made
with invasive electrophysiology, he composed new ideas leading to
major contributions in clinical cardiac electrophysiology and, more
generally, in arrhythmology. He published over 650 scientific
papers and 14 books, and had numerous functions within scientific
boards of prestigious journals. In addition he trained more than
120 cardiologists in clinical cardiac electrophysiology. On the
occasion of the congress `2000, Future of Arrhythmology: Lessons
From the Past, Promises For Tomorrow', we highlight the scientific
work of Prof. Hein J.J. Wellens. A selection of more than 60
articles over the whole time span has been selected. These articles
are accompanied by comments from an expert, co-worker and/or former
fellow in order to place the paper in a scientific time frame,
including the relationship of the author with Prof. Hein J.J.
Wellens.
The electrocardiogram (ECG) remains the most accessible and
inexpensive diagnostic tool to evaluate the patient presenting with
symptoms suggestive of acute myocardial ischemia. It plays a
crucial role in decision making about the aggressiveness of therapy
especially in relation to reperfusion therapy, because such therapy
has resulted in a considerable reduction in mortality from acute
myocardial infarction. Several factors play a role in the amount of
myocardial tissue that can be salvaged by reperfusion therapy, such
as the time interval between onset of coronary occlusion and
reperfusion, site and size of the jeopardized area, type of
reperfusion attempt (thrombolytic agent or an intracoronary
catheter intervention), presence or absence of risk factors for
thrombolytic agents, etc. Most important in decision making on
reperfusion therapy and the type of intervention is to look for
markers indicating a higher mortality rate from myocardial
infarction. The ECG is a reliable, inexpensive, non-invasive
instrument to obtain that information. Recently it has become clear
that both in anterior and inferior myocardial infarction, the ECG
frequently allows not only to identify the infarct related coronary
artery, but also the site of occlusion in that artery and therefore
the size of the jeopardized area. Obviously, the more proximal the
occlusion, the larger the area at risk and the more aggressive the
reperfusion attempt.
All physicians practicing medicine encounter patients suffering
from cardiovascular disease. This book has been outlined in such a
way that vascular surgeons, general internists, neurologists and
cardiologists should be able to use it. The book covers the
complete scope of cardiac diseases in addition to chapters on
hypertension and atherosclerosis. In many patients there is a
family history of cerebrovascular accidents, myocardial infarction
or peripheral arterial disease. Also in patients reporting collaps,
palpitations and arrhythmias the family is crucial and can provide
clues to a genetic cause of the disease. This book is published to
guide physicians in the process of determining whether a genetic
component is likely to be present. Furthermore, information is
provided what the possibilities and limitations of DNA diagnostic
techniques are. Finally, the importance of newly identified
categories of potential patients, i. e. gene carriers without
symptoms or any inducible sign of disease, is highlighted. For some
patients a genetic diagnosis is essential to determine appropriate
therapy and for counseling? In some other diseases DNA diagnostic
tools are available but the relevant for the patients may be less
clear. In other families the search for a disease causing gene is
ongoing and the possibilities to find genes and to unravel the
pathophysiology of the disease is limited by the lack of patients.
To give insight into the current state of genetic diagnostics, the
authors have classified the cardiovascular diseases.
Four years ago-in December 1997-the first European Science
Foundation Workshop on Cardiovascular Specific Gene Expression was
held in Maastricht. It was hardly possible to imagine the progress
in the field in those four years. In 1997, gene expression was
still an art focused on individual genes; in 200 I, many labs have
access to micro-array facilities to determine the expression of
thousands of genes simultaneously. In 1997, gene expression was an
area of fundamental research in basis molecular biology
laboratories; in 200 I, clinical cardiovascular research has
incorporated gene expression approaches. In 1997, the
interpretation of a gene expression experiment was usually
straightforward; in 200 I, advanced bioinformatics tools are needed
to approach the extreme complexities of genetic control of cell and
tissue function. The second symposium in this series is focused on
Cardiovascular Genomics. New Pathophysiological Concepts. The
organizing committee chose to invite a group of renown scientists
and young investigators around four topics of eminent importance in
cardiovascular research. These topics reflect the major present-day
clinical cardiovascular problems: atherosclerosis, hypertension,
arrhythmias and heart failure. In addition to these four
disease-driven topics, the workshop has sessions on gene expression
methodologies and cellular transplant approaches to cardiovascular
disease.
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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