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Current Cardiology Reviews
ISSN: 1573-403X
Current Cardiology Reviews
Volume 3, Number 4, November 2007
Contents
Etiology of the Metabolic Syndrome Pp. 232-239
Amy Z. Fan
[Abstract]
Current Concepts on Prenatal Diagnosis and Management
of Fetal Tachyarrythmias Pp. 240-254
A. Galindo and A. Mendoza
[Abstract]
Exercise Induced Cardioprotection: An Overview of
a Unique Form of Preconditioning Pp. 255-263
John C. Quindry and Karyn L. Hamilton
[Abstract]
Norepinephrine and Autonomic Modulation in Heart Failure
Pp. 264-273
Jianhua Li and Lawrence Sinoway
[Abstract]
Measurement of Physical Changes in the Myocardium
for Development of Novel Methods for Diagnosing Ischemia
Pp. 274-282
M.S. Munir, K.J. Shankar, Saeed Payvar, Hossein Eftekhari,
Alan Brewer, Jillian Robertson, Igor V. Stupin, Ed Sobash,
S. Ward Casscells and Amany Ahmed
[Abstract]
Is the Therapeutic Potential of Stem Cells for Myocardial
Regeneration Limited by Proarrhythmic Effects? Pp.
283-295
Oliver Wolfram, Matthias Hammwöhner and Andreas Goette
[Abstract]
Angiotensin Receptor Blockers in Chronic Heart Failure:
Clinical Implications and Molecular Mechanisms Pp.
296-303
Hadyanto Lim and Zhu Yi Zhun
[Abstract]
Abstracts
[Back to top]
Etiology of the Metabolic Syndrome
Amy Z. Fan
The metabolic syndrome (MSynd) refers to a clustering
of cardiovascular risk factors characterized by obesity, impaired
glucose tolerance/type 2 diabetes, atherogenic dyslipidemia,
and hypertension. The tendency that multiple risk factors
were often present in the same individual prompted researchers
to search for the underlying pathophysiology of the MSynd.
In an inventory of hypotheses on causative mechanisms for
the MSynd, plausible mechanisms include insulin re-sistance,
leptin resistance, visceral obesity, beta-cell dysfunction,
endothelial dysfunction, neuroendocrine origin (sympathetic
overactivity and vagal impairment, reduced serotonergic responsivity,
endocannabinoid system overactivity), genetic predisposition
and fetal origin. The etiology of the syndrome is complex
and each hypothesis may explain part of the etiological cascade.
More studies are needed to elucidate relevance of and relationship
between diverse hypotheses.
[Back to top]
Current Concepts on Prenatal Diagnosis and Management
of Fetal Tachyarrythmias
A. Galindo and A. Mendoza
Sustained or recurrent tachyarrhythmias are an important cause
of fetal morbidity and mortality. The most common type of
fetal tachycardia is supraventricular tachycardia, followed
by atrial flutter. Other tachyarrhythmias such as atrial ectopic
tachycardia, junctional reciprocating tachycardia and ventricular
tachycardia are rare in fetal life. Appropriate management
depends on accurate diagnosis. Ultrasound is essential for
a precise knowledge of the electrophysiologic mechanism underlying
the arrhythmia, and to examine the hemodynamic impact of the
tachycardia both before and after the antiarrhythmic therapy.
The information concerning the type of fetal tachyarrhythmia
is usually inferred from the fetal heart rate, and the relationship
between atrial and ventricular events as demonstrated by M-mode
echocardiogram and Doppler flow signals. The decision to initiate
pharmacological intervention depends on several factors and
must be weighed against possible maternal and fetal adverse
effects of the antiarrhythmic drugs. Several options are available
when facing with a fetus with a tachycardia, ranging from
close observation without therapy to direct administration
of antiarrhythmic drugs into the fetal circulation. Although
there are many series in the medical literature reporting
that fetal tachycardias can be suppressed successfully using
antiarrhythmic drugs given to the mother, currently there
is no global consensus concerning the precise management of
these fetuses. Certainly, the ultimate decision on the management
of fetal tachycardias will vary from center to center. In
this paper we will analyze our experience in the diagnosis
and management of fetal tachyarrhythmias together with a review
of modern literature in this topic.
[Back to top]
Exercise Induced Cardioprotection: An Overview of
a Unique Form of Preconditioning
John C. Quindry and Karyn L. Hamilton
Experimental models for the study of an ischemia reperfusion
(IR) resistant myocardium include exercise, ischemia, and
pharmacologic stimuli. While research utilizing all three
of these models consistently demonstrates a cardioprotected
phenotype, presently only exercise represents a viable intervention
for humans. Nonetheless, knowledge gleaned from ischemic preconditioning
research has contributed greatly to the progress in identifying
mechanisms of exercise induced cardioprotection. Similarly,
ongoing pharmacologic preconditioning investigations are a
direct byproduct of ischemic preconditioning research. In
this review we present a critical analysis of commonalities
and differences between exercise, pharmacologic, and ischemic
models of myocardial preconditioning. Specifically, we identify
keys points that illustrate why exercise research may be valuable
for translating ischemic preconditioning research into a viable
intervention against IR injury. As part of this discussion,
we first provide a brief introduction of the mechanisms responsible
for IR mediated injury followed by a thorough discussion of
exercise induced cardioprotection against IR injury.
[Back to top]
Norepinephrine and Autonomic Modulation in Heart Failure
Jianhua Li and Lawrence Sinoway
Exercise performance declines in heart failure (HF). Reduced
blood flow to active muscle has been thought to contribute
to the abnormal responses in HF. Thus it is important to understand
the mechanisms that regulate the autonomic responses during
exercise in normal subjects and in patients with HF.
Sympathetic nervous activity (SNA) is increased with exercise
in normal subjects and is increased in HF subjects at rest
and in response to exercise. Heightened peripheral SNA and
the resultant increased neurovascular levels of norepineph-rine
(NE) evoke vasoconstriction. The NE response is accentuated
in HF and this results in an increase in prominent vaso-constriction.
Interstitial concentrations of NE ([NE]i) provide an outstanding
index of NE concentrations at the neurovascular junction.
Microdialysis methods allow us to collect interstitial NE
samples from resting and active muscles of healthy control
rats and rats with HF induced by myocardial infarctions.
The completed experiments from this laboratory have shown
that NEi rises in active muscle. Several muscle metabolites
can alter the interstitial concentration of NE and in turn
influence blood flow. For example, elevated interstitial ATP
evoked by muscle stretch is linked to the rise in [NE]i. A
purinergic P2X receptor is a family of cation-permeable ligand
gated ion channels that open in response to extracellular
ATP. The elevated NE induced by muscle stimulation is attenuated
by a P2X receptor blocker, and is augmented by a nucleotidase
inhibitor. This suggests a mechanism by which NEi is increased
via P2X receptors on the sympathetic nerve terminals. K+
is also a stimulant of NE exocytosis from the sympathetic
nerve. Interstitial K+ concentration
increases with muscle contraction and K+
infused into the arterial blood supply of the hindlimb muscle
increases [NE]i. In HF, an increase in the concentration of
interstitial K+ is augmented. In addition, we have also examined
NE response to sympathetic nerve stimulation and activity
of NE uptake 1, a pathway by which NE is reabsorpted by presynaptic
sympathetic nerves. Given level of sympathetic nerve stimulation
leads to a greater NEi response in HF as compared with healthy
control. This effect is due, in part, to reduced NE uptake
1 in HF.
Our experimental results suggest that 1) ATP and P2X receptors;
2) muscle metabolite K+;
and 3) the SNA and NE uptake 1 pathway play an important role
in regulating neurovascular NE levels in HF.
[Back to top]
Measurement of Physical Changes in the Myocardium
for Development of Novel Methods for Diagnosing Ischemia
M.S. Munir, K.J. Shankar, Saeed Payvar, Hossein Eftekhari,
Alan Brewer, Jillian Robertson, Igor V. Stupin, Ed Sobash,
S. Ward Casscells and Amany Ahmed
The purpose of this review is to offer a concise discussion
of existing data describing changes in the physical properties
of the myocardium in response to ischemia. We argue that these
measurable changes may be used as a basis for the development
of newer diagnostic methods. Because of the challenges involved
in the timely and accurate diagnosis of ischemia, newer methods—or
those that will complement existing methods—are needed.
Altered physical property surveillance encompasses concepts
and theories that may be utilized for developing methods for
detecting ischemia by sensing the resultant changes in the
physical properties of the myocardium.
[Back to top]
Is the Therapeutic Potential of Stem Cells for Myocardial
Regeneration Limited by Proarrhythmic Effects?
Oliver Wolfram, Matthias Hammwöhner and Andreas Goette
Stem cells have recently gained attention within Cardiology
for their therapeutical application as a treatment in acute
myocardial infarction and heart failure. Especially for larger
infarct areas, direct myocardial application of bone-marrow
derived progenitor cells or the subcutaneous treatment with
colony-stimulating factors seems to lead to a small, but noticeable
improvement of left ventricular performance. Given this current
example of wider therapeutic use of stem cells and progenitor
cells it seems warranted to take a closer look at the safety
profile of this novel approach. Proarrhythmic properties of
embryonic stem cells have already been reported several years
ago, yet evidence is lacking that these experimental features
are of relevance for daily clinical use of adult stem cells.
This review will focus on the available data regarding the
proarrhythmic potential of stem cell application based on
the available experimental and clinical electrophysiologic
data.
[Back to top]
Angiotensin Receptor Blockers in Chronic Heart Failure:
Clinical Implications and Molecular Mechanisms
Hadyanto Lim and Zhu Yi Zhun
Angiotensin II is the main effector molecule of the renin-angiotensin
system and has been implicated in regulating cell growth,
inflammation and fibrosis, contributing to cardiac remodeling,
growth and apoptosis. Cardiac remodeling is the determinant
in the progression of heart failure. Thus, chronic activation
of the renin-angiotensin system plays an important role in
the structural and functional pathogeneses of heart failure.
To date, most of the known physiological effects of Ang II
in adult tissues are attributable to the AT1R
although recent progress has shown some important actions
of the involvement of AT2R.
Clinical trials have documented consistent mortality and morbidity
benefits of angiotensin receptor blockers in patients with
chronic heart failure. Recent experimental studies link the
beneficial effects of inhibiting Ang II to transforming growth
factor-β1.
Extracellular matrix accumulation in cardiovascular system
is involved in vascular and cardiac hypertrophy and heart
failure. Therefore, Ang II and TGF-β1
cross talk provides the pathophysiological insight in the
development of cardiac fibrosis and heart failure. These molecular
interactions might provide the beneficial effects of chronic
AT1 receptor blockade, a
known antifibrotic strategy, in patient with heart failure.
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