Peter Magnusson

By Peter Magnusson

Hypertrophic cardiomyopathy (HCM) affects 1:500 individuals, and in majority of cases, a mutation in sarcomere proteins can explain the disease. Phenotype is heterogeneous and thus the prognosis. Many patients suffer from dyspnoea, especially at exercise. Unfortunately, sudden cardiac death (SCD) does occur at all ages and is a major cause of death in young adults. There is no proven pharmacological treatment to reduce hypertrophy or fibrosis, but beta-blockers are first-line treatment. In patients with obstruction, myectomy is preferred in the young, but in older patients, alcohol septal ablation is tried to reduce symptoms and possibly prognosis. Risk stratification of sudden cardiac death is challenging. The major established risk factors are extreme myocardial thickness, non-sustained ventricular tachycardia, unexplained syncope, abnormal exercise blood pressure response, and family history of sudden cardiac death. In 2014, a novel risk calculator was developed that also takes age, outflow gradient, and left atrial seize into account. Implantable defibrillator treatment is effective in HCM, but complications requiring surgery and inappropriate shocks remain a problem.

Part of the book: Cardiomyopathies

By Burhan Sheikh Alkar, Gustav Mattsson and Peter Magnusson

Ischemic cardiomyopathy, disease of the heart muscle due to coronary artery disease, is the most common cardiomyopathy. It is often difficult to discern the etiology of heart failure, and often there are multiple underlying causes. Ischemic cardiomyopathy most often presents with a dilated morphology with wall motion defects and a history of previous myocardial infarction or confirmed coronary artery disease. Mechanisms of myocardial depression in ischemia are necrosis of myocardial cells resulting in irreversible loss of function or reversible damage, either short term through myocardial stunning or long term through hibernation. In ischemic cardiomyopathy, echocardiography may be extended with stress testing or other imaging modalities such as myocardial scintigraphy and cardiac magnetic resonance tomography. Coronary angiography is often considered a gold standard; however, other modalities such as positron emission tomography can be needed to detect small vessel disease. Cardiac revascularization, through percutaneous coronary intervention and coronary artery bypass grafting, both in acute coronary syndrome and in stable coronary artery disease, relieves symptoms and improves prognosis. Therapy should aspire to treat ischemia, arrhythmias in addition to heart failure management, which includes device therapy with cardiac resynchronization therapy, implantable cardioverter defibrillators, and mechanical support as bridging or destination therapy in end-stage disease.

Part of the book: Current Perspectives on Cardiomyopathies

By Måns Almqvist, Gustav Mattsson, Robin Razmi and Peter Magnusson

The use of cardiac devices, that is, pacemakers and implantable cardioverter defibrillators, has increased, and the incidence will likely continue to increase due to an aging population with associated risk factors. Unfortunately, this implies an increasing number of complications, including infections. Cardiac device-related infection is a dreaded complication causing both increased morbidity and mortality, and considerable costs. Because of the presence of a foreign body in subcutaneous tissue, vasculature, and the heart, patients with cardiac device systems are at increased risk of endocarditis due to microbial agents. In general, an infected device system should be removed in its entirety. The timing of reimplantation varies due to indication and severity of the infection. Furthermore, the explant procedure may be complicated and should be performed by an experienced team including facilities to handle life-threatening complications. The subcutaneous implantable cardioverter defibrillator or leadless pacemaker can serve as an option in selected cases. This chapter will describe clinical aspects of cardiac device-related infections.

Part of the book: Infective Endocarditis

By Peter Magnusson

Part of the book: Aortic Stenosis

By Robin Razmi and Peter Magnusson

Part of the book: Infective Endocarditis