Future cardiology
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Despite a crucial role in body fluid homeostasis, elevated vasopressin levels can also be pathological in conditions such as congestive heart failure, liver cirrhosis and the syndrome of inappropriate antidiuretic hormone secretion. The result of elevated vasopressin is renal water retention and hyponatremia, a low serum sodium concentration. Hyponatremia is associated with excess morbidity and mortality. ⋯ Selective V2- and combined V1a/V2-receptor antagonists have been developed for the treatment of hyponatremia resulting from congestive heart failure, liver cirrhosis and the syndrome of inappropriate antidiuretic hormone secretion. Two nonpeptide vasopressin-receptor antagonists, conivaptan and tolvaptan, have recently been approved by American and European drug authorities for clinical use. This article aims to provide a succinct and clinical update on nonpeptide vasopressin-receptor antagonists, including their mechanism of action, performance in randomized clinical trials and current clinical status.
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Sudden cardiac death, secondary to malignant ventricular arrhythmias, has traditionally been associated with structural heart disease. An important exception includes a group of clinical entities referred to as 'channelopathies' that develop secondary to genetic mutations, which alter cardiac ion channel activity. Otherwise healthy individuals affected by these forms of primary electrical disease are vulnerable to fatal arrhythmic events from a very young age. ⋯ Our growing insight into the genetics of these conditions has led to an improved understanding of the molecular pathophysiology responsible for the malignant arrhythmias characterizing these disorders. However, despite our knowledge of these conditions, the success of medical therapy remains modest and the prevention of sudden cardiac death may necessitate insertion of an implantable cardioverter-defibrillator. The young age of affected patients makes this a particularly undesirable treatment strategy and emphasizes the importance of translating our insight into the molecular pathophysiology defining these conditions into more effective forms of therapy.
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The use of epinephrine during cardiac arrest has been advocated for decades and forms an integral part of the published guidelines. Its efficacy is supported by animal data, but human trial evidence is lacking. This is partly attributable to disparities in trial methodology. ⋯ One possible explanation for the lack of epinephrine's demonstrated efficacy in human trials of out-of-hospital cardiac arrest is the delay in its administration. A potential solution may be intraosseus epinephrine, which can be administered quicker. More importantly, it is the quality of the basic life support, early and uninterrupted chest compressions, early defibrillation and postresuscitation care that will provide the best chance of neurologically intact survival.
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Aortic valve disease is a growing cause of mortality and morbidity, especially in developed countries. Whereas medical therapy is associated with an ominous prognosis, since the 1970s, surgical valve replacement has represented a standard therapy for fit patients. Indeed, this approach is safe and feasible in younger patients without comorbidities. ⋯ The advent of transcatheter valve replacement techniques, by means of percutaneous or transapical approaches, has been recently introduced into mainstream clinical practice and is likely to radically change the treatment of aortic valve disease. At present, further data are needed to thoroughly appraise the long-term risk-benefit balance of transcatheter valve replacement techniques. For this reason, it can only be considered for high surgical risk patients, but early results are so promising that in the future, transcatheter aortic valve implantation could became the first therapeutic choice, even for low-risk patients.
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Studies with recently introduced point-of-care (POC) platelet function tests have shown that individuals are variably responsive to aspirin and clopidogrel therapy, and that hyporesponsiveness to antiplatelet therapy is associated with an increased risk of cardiovascular events. However, the currently available POC tests have undergone only limited clinical evaluation and clinicians are uncertain about the best POC test, the optimal cut-off point to define hyporesponsiveness in different patient populations and clinical settings, the appropriate management of patients demonstrating hyporesponsiveness and the cost effectiveness of adjusting treatment on the basis of the results of POC platelet function testing. Several large randomized controlled trials currently underway are examining whether adjusting antiplatelet therapy on the basis of a POC test result can improve patient-important outcomes. Until these issues are resolved, POC testing to monitor antiplatelet therapy will largely remain a research tool and patients should continue to receive oral antiplatelet therapy without routine monitoring at doses that have been demonstrated to be effective in randomized controlled trials.