67 research outputs found
Sexual function in hypertensive patients receiving treatment
No full textThorsten Reffelmann, Robert A KlonerUniversity of Southern California, The Heart Institute, Good Samaritan Hospital, Division of Cardiovascular Medicine, Keck School of Medicine, Los Angeles, CA, USAAbstract: In many forms of erectile dysfunction (ED), cardiovascular risk factors, in particular arterial hypertension, seem to be extremely common. While causes for ED are related to a broad spectrum of diseases, a generalized vascular process seems to be the underlying mechanism in many patients, which in a large portion of clinical cases involves endothelial dysfunction, ie, inadequate vasodilation in response to endothelium-dependent stimuli, both in the systemic vasculature and the penile arteries. Due to this close association of cardiovascular disease and ED, patients with ED should be evaluated as to whether they may suffer from cardiovascular risk factors including hypertension, cardiovascular disease or silent myocardial ischemia. On the other hand, cardiovascular patients, seeking treatment of ED, must be evaluated in order to decide whether treatment of ED or sexual activity can be recommended without significantly increased cardiac risk. The guideline from the first and second Princeton Consensus Conference may be applied in this context. While consequent treatment of cardiovascular risk factors should be accomplished in these patients, many antihypertensive drugs may worsen sexual function as a drug specific side-effect. Importantly, effective treatment for arterial hypertension should not be discontinued as hypertension itself may contribute to altered sexual functioning; to the contrary, alternative antihypertensive regimes should be administered with individually tailored drug regimes with minimal side-effects on sexual function. When phosphodiesterase-5 inhibitors, such as sildenafil, tadalafil and vardenafil, are prescribed to hypertensive patients on antihypertensive drugs, these combinations of antihypertensive drugs and phosphodiesterase 5 are usually well tolerated, provided there is a baseline blood pressure of at least 90/60 mmHg. However, there are two exceptions: nitric oxide donors and α-adrenoceptor blockers. Any drug serving as a nitric oxide donor (nitrates) is absolutely contraindicated in combination with phosphodiesterase 5 inhibitors, due to significant, potentially life threatening hypotension. Also, α-adrenoceptor blockers, such as doxazosin, terazosin and tamsulosin, should only be combined with phosphodiesterase 5 inhibitors with special caution and close monitoring of blood pressure. Keywords: Sexual function, erectile dysfunction, hypertension, antihypertensive therapy, phosphodiesterase 5 inhibitor
Schädigung der mikrovaskulären Durchblutung nach myokardialer Ischämie und Reperfusion : Einflussgrößen, Behandlungsansätze und prognostische Relevanz des No-Reflow-Phänomens am Herzen
No full textSchädigung der mikrovaskulären Durchblutung nach myokardialer Ischämie und Reperfusion : Einflussgrößen, Behandlungsansätze und prognostische Relevanz des No-Reflow-Phänomens am Herzen
No full textBedeutung der endogenen Aktivierung von ATP-sensitiven K + -Kanälen beim frühen hypoxischen Herzversagen für Kontraktilität und Energiestatus des Myokards : Beeinflußbarkeit im Sinne einer Kardioprotektion ; mechanisch-funktionelle, elektrophysiologische und energetisch-NMR-spektroskopische Untersuchungen
No full textBedeutung der endogenen Aktivierung von ATP-sensitiven K + -Kanälen beim frühen hypoxischen Herzversagen für Kontraktilität und Energiestatus des Myokards : Beeinflußbarkeit im Sinne einer Kardioprotektion ; mechanisch-funktionelle, elektrophysiologische und energetisch-NMR-spektroskopische Untersuchungen
No full textAdjunctive Reperfusion Therapy Post-AMI
No full text• Reperfusion of the occluded coronary artery in an ST-segment-elevation myocardial infarction is the most effective approach for reducing infarct size, preserving left ventricular ejection fraction, lowering the incidence and severity of congestive heart failure and improving prognosis• Hence, several pharmacologic agents intended to improve target vessel patency as an adjunct to thrombolysis or primary percutaneous coronary intervention have been shown to be beneficial in patients with reperfusion therapy for acute myocardial infarction, namely antiplatelet and anticoagulation agents• Animal investigations have suggested that coronary reperfusion may also result in undesirable cardiac alterations, termed ‘reperfusion injury’, such as reversible contractile dysfunction (‘stunning’), microvascular obstruction (‘no-reflow’), and in several studies the progression of myocardial necrosis (‘lethal reperfusion injury’)• Clinical investigations of various pharmacologic interventions as an adjunctive therapy to reperfusion to reduce final infarct size, the amount of contractile dysfunction and to improve prognosis have been mostly inconsistent; only a few interventions, e.g. adenosine and atrial natriuretic peptide seem to show promise at least in certain subgroups.</p
Blood supply of the graft after cellular cardiomyoplasty
No full text Cellular cardiomyoplasty is under extensive investigation as a potential therapeutic strategy after myocardial infarction, in congestive heart failure and chronic ischemic heart disease. Various cell sources and techniques for transplantation have been studied in animal models of cardiac disease. The initial goal of replacing myocardial scar tissue by vital myocardial cells, integrated into the host, simultaneously beating and contributing to systolic force, has not yet been accomplished. However, most experimental models provided evidence for enhanced vascularization after cell transplantation. In some investigations, neovascularization was also shown to be accompanied by increased myocardial perfusion. Mechanisms by which vascularization occurs have not been fully elucidated: either the transplanted cells provide an angiogenic stimulus, involving various paracrine or hormone-like factors, which induces the formation of a new vasculature or, depending on the source of transplanted cells, the cells incorporate into the vascular network after proliferation and differentiation. This review summarizes research that specifically studied the occurrence, magnitude and mechanisms of enhanced myocardial blood supply after cellular cardiomyoplasty </jats:p
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