Future cardiology
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A substantial proportion of patients who undergo cardiac rhythm device implantation receive anticoagulation to prevent thromboembolism. Many patients have coexisting cardiovascular diseases treated with antiplatelet therapy. Anticoagulation may increase the risk of hemorrhagic complication, while withdrawal of anticoagulation may increase thromboembolic risk. In this article, we review and describe the available evidence, in order to inform best practice .
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Despite advancements in surgical techniques over the past 20 years, Fontan patients have decreased exercise capacity as a consequence of an inherent inability to adequately increase cardiac output during exercise. They are also affected by several complications that are associated with considerable morbidity and mortality. ⋯ In Fontan circulation, pulmonary vascular resistance is the single most important factor involved in the limitation of cardiac output and treatments able to decrease pulmonary vascular resistance might conversely improve cardiac output and exercise capacity. In this article we discuss the initial experience with the use of sildenafil in Fontan patients and we discuss the possible mechanisms through which sildenafil might positively act in Fontan circulation.
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The treatment of heart failure has seen considerable advances in the past decades. In particular, a therapeutic focus on the renin-angiotensin-aldosterone system has provided significant improvements in outcomes. Multiple inhibition points in the renin-angiotensin-aldosterone system, including direct renin inhibitors, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and mineralocorticoid receptor antagonists, have the common feature of either blocking aldosterone production (direct renin inhibitor, angiotensin-converting enzyme inhibitor, angiotensin receptor blocker) or the mineralocorticoid receptor. ⋯ Interventions to reliably control serum K(+) during renin-angiotensin-aldosterone inhibition have not been available to date, and would be of particular value with the use of mineralocorticoid receptor antagonists that have been shown to reduce mortality in patients with heart failure and a reduced left ventricular ejection fraction. In this review, we examine the PEARL-HF study, which has tested the combined use of RLY5016, a novel nonabsorbed K(+) binding polymer, with spironolactone in heart failure patients receiving standard care but with previous documented hyperkalemia or chronic kidney disease. RLY5016 significantly lowered serum K(+) levels from baseline relative to placebo, lowered the incidence of hyperkalemia and allowed a higher proportion of heart failure patients to receive spironolactone at a dose of 50 mg/day.
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Patients who continue to suffer from severe and disabling angina pectoris, despite optimum treatment in terms of conventional pharmacological therapy and/or revascularization procedures, have been termed as having refractory angina pectoris. The future group of patients with refractory angina pectoris will be different from today's patients and represent a 'moving target' as risk factors, efficacy of treatment and indications continue to change. ⋯ There is strong evidence for SCS giving symptomatic benefits (decrease in anginal attacks), improved quality of life and improvement of functional status. In addition, SCS seems to be cost effective with a 'break-even' after approximately 15-16 months.
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Kounis syndrome is the concurrence of acute coronary syndromes with conditions associated with mast cell activation, such as allergies or hypersensitivity and anaphylactic or anaphylactoid insults that can involve other interrelated and interacting inflammatory cells behaving as a 'ball of thread'. It is caused by inflammatory mediators such as neutral proteases including tryptase and chymase, arachidonic acid products, histamine, platelet activating factor and a variety of cytokines and chemokines released during the activation process. Platelets with FCεRI and FCεRII receptors also participate in the above cascade. ⋯ Kounis syndrome has revealed that the same mediators released from the same inflammatory cells are present in acute coronary events of nonallergic etiology. These cells are not only present in the culprit region before plaque erosion or rupture but they release their contents just before an actual coronary event. Therefore, does Kounis syndrome represent a magnificent natural paradigm and nature's own experiment in a final trigger pathway implicated in cases of coronary artery spasm and plaque rupture showing a novel way towards our effort to prevent acute coronary syndromes? Drugs, substances targeting the stem cell factor that is essential for mast cell development, proliferation, survival, adhesion and homing as well as monoclonal antibodies and natural molecules that protect mast cell surface and stabilize mast cell membrane could emerge as novel therapeutic ways capable to prevent acute coronary and acute cerebrovascular events.