309 research outputs found
Levels of evidence in the European Society of Cardiology Guidelines: Gaps in knowledge?
No full textNo abstract availabl
Pathophysiological role of heart rate: from ischaemia to left ventricular dysfunction
No full textMyocardial ischaemia results from imbalance between myocardial oxygen demand and
supply. An increase in heart rate (HR) will raise both demand and supply. HR is the
most important determinant of myocardial oxygen consumption and of cardiac
energy demand. HR reduction improves myocardial perfusion by increasing the fraction
of the cardiac cycle occupied by diastole, which accounts for 80% of coronary
flow. Besides these physiological characteristics, HR is also linked to the progression
of atherosclerosis, at least in animals, and an increase in HR is associated with
plaque rupture in humans. The symptom of chest pain in stable angina is almost
always triggered by elevated HR owing to physical or emotional stress. Equally, an
increased HR precedes an episode of asymptomatic or silent myocardial ischaemia.
Therefore, it is not surprising that the efficacy of some anti-anginal drugs such as
b-blockers and non-dihydropyridine calcium antagonists has been related to their
effectiveness in reducing HR. In many studies, multivariate analysis has shown HR
to be an independent predictor of mortality and of hospitalization for heart failure.
A relationship has been found between HR reduction and mortality in patients with
congestive heart failure treated with b-blockers. Thus HR is an important therapeutic
target for ischaemia and left ventricular dysfunction or congestive heart failure, and it
seems likely that relatively high HR is both causative and indicative of important
pathophysiological processes: HR is a risk factor for cardiovascular morbidity and
mortality throughout the cardiovascular continuu
A way forward to the elimination of conflict of interest for experts involved in regulatory medicine and guidelines
No full textOne must always be aware that external influences may affect the
interpretation of study results, the process of drug approval, and
the economical analyses of pharmaceutical agents. Companies
often have an important say in the definition of the research question,
in the selection of patients, the way of reporting drop-outs, and
adverse events. Furthermore, industry-financed cost-effectiveness
analyses are more likely to support additional expenditures on investigational
drugs than standard treatments.On the other hand, we have to recognize the pivotal role of the
pharmaceutical industry in biomedical research since, given the lack
of public funding, the majority of funded clinical trials in Europe and
in the Americas is supported by industry. There are examples of
government-funded clinical trials that changed the course of a
disease, but they are scanty
Effect of thalidomide on the skeletal muscle in experimental heart failure
No full textEur J Heart Fail. 2002 Aug;4(4):455-60.
Effect of thalidomide on the skeletal muscle in experimental heart failure.
Vescovo G, Ravara B, Angelini A, Sandri M, Carraro U, Ceconi C, Dalla Libera L.
Internal Medicine, Adria Hospital, Italy. [email protected]
Abstract
BACKGROUND:
Tumour Necrosis Factor alpha (TNFalpha) has been shown to contribute to heart failure (CHF) progression.
AIMS:
We have tried to antagonise the detrimental effects of TNFalpha on skeletal muscle apoptosis, by using thalidomide, a drug that inhibits its biosynthesis.
METHODS:
CHF was induced in 20 rats by injecting monocrotaline, which determines right ventricle (RV) failure. After 2 weeks, when CHF developed, 12 rats were treated with thalidomide 3.5.mg/kg per day for 2 weeks. Eight had saline and served as CHF controls.
RESULTS:
Thalidomide failed to decrease TNFalpha and its second messenger sphingosine (SPH), but was able to prevent the shift toward the fast myosin heavy chains. In the Tibialis Anterior muscle of the thalidomide group, the degree of atrophy, the number of apoptotic nuclei and the levels of caspases, were similar to those of the CHF controls.
CONCLUSIONS:
Thalidomide, at the doses used in this study, which are the same employed for the treatment of tubercolosis, leprosy, AIDS and cancer in humans, did not lower either TNFalpha or SPH and only marginally influenced the apoptosis-induced muscle atrophy. Since other TNFalpha blockers are under investigation for improving the clinical status of patients with CHF, the present data could be relevant in the design of randomised clinical trials in humans.
PMID:
12167383
[PubMed - indexed for MEDLINE
Dallo scompenso alla cardiopatia ischemica: i nuovi target terapeutici dell’inibizione del sistema renina-angiotensina.
No full text
INIBIZIONE SELETTIVA E SPECIFICA DEI CANALI IF CON UNA NUOVA MOLECOLA PER LA TERAPIA DELLE MALATTIE CARDIOVASCOLARI / SELECTIVE AND SPECIFIC IF INHIBITION WITH NEW MOLECULE: NEW PERSPECTIVES FOR THE TREATMENT OF CARDIOVASCULAR DISEASE
No full textLdaia Fcroe qedu eunnz aa uCmaredniatoc ad (eFllCa )f rèe quune enlzeam ceanrtdoia dceat perumò indaivnetnet adreel lcao cnasuusma osc dait eonsasingteen fios idoepl amtouloscgoicloa dcaerl-- ln’ieslclah emmailaa tmtiaio ccaarrddiiocvaa. sLc’oaluamree. nLtaa stcao fpreeqrtuae en zl’aa pcparlidciaazciao nae rciplinoiscoa èd ic uonnas idneuroavtaa muno lfeactotolar ec hdei aribscbhaiso- rsoa nlaa rFicCa h(aC AdiDm) oes tnraetlloo cshceo mqupeesntsao è caanrdchiaec ou n( SimC)p. oErftfaentttiev aombeienttteiv,o i ln deel ctrreamttaemnteon tdoe ldlae lflrae mquaelantztaia c caor-- ldai arcicah oietsttean udti oo scsoigne qnuoe dsteol mnuioocvaor dfaiorm, aaucmo,e unnta i nlaib piteorrfue ssioelneett idvioa seto slpiceac eifi cmoi gdleiollraa cl’oarprepnotreto I fe, nriedrugcee- ztiicoon ea l vmeniotrciacrodlaiore i sscihneismtraic on.e Lll’oIv aSbCr,a ed inriad upcreo tiel grgime oild melliaomcaerndtioo dmuiroacnatred ilc’iosc choenmsieag, umenigtleio arall ’ilna ffaurtno- caacrudtoia.c Ma ?ig7l0io brap mla , psriao gnneoi psia sziiae nntei ic ponaz SieCn tei dcoisnfu CnzAioDn, ed diseful nvezinotnriec ovleon stirnicisotlraor.e L s’Iivnaisbtrraad, ien afr èe quune nfazra- mmaalcaot tsiaic cuarord, iobveans ctoolllaerrea.t
Differenti siti di azione del diltiazem, nifedipina e verapamil sul miocardio e sulla muscolatura liscia aortica e coronarica.
No full textLink between chronic obstructive pulmonary disease and coronary artery disease: implication for clinical practice
No full textChronic obstructive pulmonary disease (COPD) and coronary artery disease (CAD) are global epidemics that incur significant morbidity and mortality. These diseases are frequently found in combination, and they can also be found independent of the common causal factors, primarily smoking. Both conditions are systemic disorders with overlapping mechanisms and pathophysiologic processes. CAD has a strong effect on the severity and prognosis of COPD and vice versa, including acute exacerbations. Even the most recent practical clinical recommendations driven by Clinical Practice Guidelines still focus on one disease at a time, and do not provide advice for the management of patients with associated chronic conditions. COPD should be approached in a more comprehensive manner, including the treatment of cardiac comorbidities, particularly CAD. To focus treatment on these comorbidities might modify the natural course of the disease in patients with COPD who may not find relief from treatment of COPD alone
- …
