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Current
Cardiology Reviews
ISSN: 1573-403X
OPEN ACCESS PLUS
Contents
Cardiac Innervation and Sudden Cardiac Death,
2009, 5, 289-295
Masaki Ieda and Keiichi Fukuda
[Abstract] [Full
Text Article]
Anaerobic Bacteria as a Cause of Mycotic Aneurysm
of the Aorta: Microbiology and Antimicrobial Therapy,
2009, 5, 36-39
Itzhak Brook
[Abstract] [Full
Text Article]
Endothelial Progenitor Cells Dysfunction and Senescence:
Contribution to Oxidative Stress, 2008, 4, 275-286
Toshio Imanishi, Hiroto Tsujioka and Takashi Akasaka
[Abstract] [Full
Text Article]
The Real Code of Leonardo da Vinci, 2008,
4, 60-62
Leiv Ose
[Abstract] [Full
Text Article]
Etiology of the Metabolic Syndrome, 2007,
3, 232-239
Amy Z. Fan
[Abstract] [Full
Text Article]
Is Type D Personality Here to Stay? Emerging Evidence
Across Cardiovascular Disease Patient Groups, 2006,
2, 205-213
Susanne S. Pedersen and Johan Denollet
[Abstract] [Full
Text Article]
Abstracts
[Back to top]
Cardiac Innervation and Sudden Cardiac Death
Masaki Ieda and Keiichi Fukuda
[Full
Text Article]
The heart is extensively innervated and its performance is
tightly controlled by the nervous system. Cardiac innervation
density varies in diseased hearts leading to unbalanced neural
activation and lethal arrhythmia. Diabetic sensory neuropathy
causes silent myocardial ischemia, characterized by loss of
pain perception during myocardial ischemia, which is a major
cause of sudden cardiac death in diabetes mellitus (DM). Despite
its clinical importance, the mechanisms underlying the control
and regulation of cardiac innervation remain poorly understood.
We found that cardiac innervation is determined by the balance
between neural chemoattractants and chemorepellents within
the heart. Nerve growth factor (NGF), a potent chemoattractant,
is induced by endothelin-1 upregulation during development
and is highly expressed in cardiomyocytes. By comparison,
Sema3a, a neural chemorepellent, is highly expressed in the
subendocardium of early stage embryos, and is suppressed during
development. The balance of expression between NGF and Seme3a
leads to epicardial-to-endocardial transmural sympathetic
innervation patterning. We also found that downregulation
of cardiac NGF leads to diabetic neuropathy, and that NGF
supplementation rescues silent myocardial ischemia in DM.
Cardiac innervation patterning is disrupted in Sema3a-deficient
and Sema3aoverexpressing mice, leading to sudden death or
lethal arrhythmias. The present review focuses on the regulatory
mechanisms underlying cardiac innervation and the critical
role of these processes in cardiac performance.
[Back to top]
Anaerobic Bacteria as a Cause of Mycotic Aneurysm
of the Aorta: Microbiology and Antimicrobial Therapy
Itzhak Brook
[Full
Text Article]
This review summarizes the microbiology, and antimicrobial
management of mycotic aneurysm of the aorta (MAA) due to anaerobic
bacteria. Anaerobic bacteria are an uncommon but important
cause of MAA. Most cases of anaerobic MAA are caused anaerobic
gram-negative bacilli (mostly B. fragilis group),
Clostridium spp. (mostly Clostridium septicum,
and Propionobacterium spp. (mostly P. acnes).
Clostridial infection is frequently associated with gastrointestinal
or hematologic malignancy. A review of all the reported cases
is presented. Treatment of MAA involving anaerobic bacteria
includes the use of antimicrobial effective against these
organisms.
[Back to top]
Endothelial Progenitor Cells Dysfunction and Senescence:
Contribution to Oxidative Stress
Toshio Imanishi, Hiroto Tsujioka and Takashi Akasaka
[Full
Text Article]
The identification of endothelial progenitor cells (EPCs)
has led to a significant paradigm in the field of vascular
biology and opened a door to the development of new therapeutic
approaches. Based on the current evidence, it appears that
EPCs may make both direct contribution to neovascularization
and indirectly promote the angiogenic function of local endothelial
cells via secretion of angiogenic factors. This concept
of arterial wall repair mediated by bone marrow (BM)-derived
EPCs provided an alternative to the local “response
to injury hypothesis” for development of atherosclerotic
inflammation. Increased oxidant stress has been proposed as
a molecular mechanism for endothelial dysfunction, in part
by reducing nitric oxide (NO) bioavailability. EPCs function
may also be highly dependent on a well-controlled oxidant
stress because EPCs NO bioavailability (which is highly sensitive
to oxidant stress) is critical for their in vivo
function. The critical question is whether oxidant damage
directly leads to an impairment in EPCs function. It was revealed
that activation of angiotensin II (Ang II) type 1 receptor
stimulates nicotinamide-adenine dinucleotide phosphate (NADPH)
oxidase in the vascular endothelium and leads to production
of reactive oxygen species. We observed that Ang II accelerates
both BM- and peripheral blood (PB)-derived EPCs senescence
by a gp91phox-mediated increase of oxidative stress, resulting
in EPCs dysfunction. Consistently, both Ang II receptor 1
blockers (ARBs) and angiotensin converting enzyme (ACE) inhibitors
have been reported to increase the number of EPCs in patients
with cardiovascular disease. In this review, we describe current
understanding of the contributions of oxidative stress in
cardiovascular disease, focusing on the potential mechanisms
of EPCs senescence.
[Back to top]
The Real Code of Leonardo da Vinci
Leiv Ose
[Full
Text Article]
Leonardo da Vinci was born in Italy. Among the researchers
and scientists, he is favourably known for his remarkable
efforts in scientific work. His investigations of atherosclerosis
judiciously combine three separate fields of research. In
1506, he finished his masterpiece, painting of Mona Lisa.
A careful clinical examination of the famous painting reveals
a yellow irregular leather-like spot at the inner end of the
left upper eyelid and a soft bumpy well-defined swelling of
the dorsum of the right hand beneath the index finger about
3 cm long. This is probably the first case of familial hypercholesterolemia
(FH). The FH code of Leonardo da Vinci was given immense consideration
by scientists like Carl Muller, who described the xanthomas
tuberosum and angina pectoris. On the contrary, Akira Endo
searched for microbial metabolites that would inhibit HMG-CoA
reductase, the rate-limiting enzyme in the synthesis of cholesterol
and finally, Michael Brown and Joseph Goldstein published
a remarkable series of elegant and insightful papers in the
70s and 80s. They established that the cellular uptake of
low-density lipoprotein (LDL) essentially requires the LDL
receptor. In conclusion: this was the real Code of Leonardo
da Vinci.
[Back to top]
Etiology of the Metabolic Syndrome
Amy Z. Fan
[Full
Text Article]
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]
Is Type D Personality Here to Stay? Emerging Evidence
Across Cardiovascular Disease Patient Groups
Susanne S. Pedersen and Johan Denollet
[Full
Text Article]
The distressed personality (Type D) is an emerging risk
factor in cardiovascular disease (CVD) that incurs a risk
on par with left ventricular dysfunction in patients with
ischemic heart disease. Type D is defined as the co-occurring
tendencies to experience increased negative emotions and to
inhibit self-expression in social interactions. Evidence is
accumulating that Type D may also be a risk factor for adverse
outcome across CVD patient groups, including patients undergoing
revascularization with drug-eluting stent implantation or
bypass surgery, patients with heart failure, peripheral arterial
disease, and arrhythmia. In these patient groups, Type D personality
has been associated with a 2-5 fold increased risk of adverse
prognosis, impaired quality of life and symptoms of anxiety
and depression independent of traditional biomedical risk
factors, including disease severity. Although little is known
about the pathways responsible for the detrimental effects
of Type D on clinical outcome, the immune system and health-related
behaviors, such as smoking and non-compliance, are likely
candidates. Further research is warranted to investigate whether
Type D personality is here to stay as a risk factor for CVD,
but weighing current evidence on Type D against a set of external
criteria shows that Type D personality fulfills the majority
of these criteria. Importantly, Type D can easily be assessed
in clinical research and practice with the standardized and
validated DS14.
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