Common cardiac conditions, drugs and methods of assessment
Judy Bothamley, Maureen Boyle in Medical Conditions Affecting Pregnancy and Childbirth, 2020
Aortic regurgitation occurs when the aortic valve does not close properly and blood leaks back into the left ventricle (seeFigure 3.2). This backflow can lead to a left ventricular volume overload, with the heart having to work harder with each heartbeat, and may result in heart failure. It can be due to congenital abnormality of valves, rheumatic fever, endocarditis or systemic vasculitis – for example, rheumatoid arthritis or systemic lupus erythematosus (SLE) (Elkayam and Bitar, 2005). It is usually well tolerated in pregnancy. If symptomatic with left ventricular dysfunction, drug therapy may be needed. Antibiotics are usually prescribed for labour. In the postnatal period a residual valve dilation may result from the pregnancy, and this will need observation, monitoring and, perhaps, surgery.
The heart
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella in Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Two major types of changes are commonly seen with heart valve disease: stenosis and incompetence. Stenosis is a narrowing of the valve opening due to thickening of the valve cusps. Stenosis may result from scaring of the valves that occurs from rheumatic fever or from a congenital malformation in the valve. The result of stenosis is a turbulent blood flow that leads to decreased efficiency of blood pumping and an increased workload on the chamber that is pumping. Aortic stenosis affects the aortic semilunar valve and reduces blood flow from the left ventricle into the aorta. Mitral stenosis affects the mitral valve, located between the atria and ventricles, and reduces blood flow between those two chambers. Incompetent or regurgitant valves are heart valves that fail to shut completely and therefore allow blood to flow to continue even when closed. Valves may become incompetent after being damaged by rheumatic fever or as a result of congenital mitral valve prolapse (see figure d above). With aortic regurgitation, the aortic semilunar valve fails to shut properly and some blood flows back into the left ventricle after contraction. Mitral regurgitation is characterized by a backflow of blood from the left ventricle into the left atrium during contraction.
Diseases of the aorta
Swati Gupta, Alexandra Marsh, David Dunleavy, Kevin Channer in Cardiology and the Cardiovascular System on the move, 2015
signs and symptomsOften patients are asymptomatic with no clinical signs.May experience bouts of pain (the nature and site of pain depend on the location of the aneurysm).Hoarseness (may result due to stretching of the recurrent laryngeal nerve).Often hypertensive.Symptoms and signs of aortic regurgitation (may result from aortic root dilatation).
TAVR in Patients with Left Ventricular Assist Device: Case Report and Literature Review
Published in Structural Heart, 2019
Alessandro Iadanza, Flavio D’Ascenzi, Andrea Torrisi, Giuseppe Sinicropi, Eugenio Neri, Sonia Bernazzali, Massimo Maccherini, Carlo Pierli
Aortic regurgitation (AR) is one of these complications; approximately one third of patients develop mild-to-moderate AR around 6 months after implantation.4 The etiology of AR associated with LVAD with continuous flow is due to several factors (Figure 1), including the reduced opening of the aortic valve, the altered dynamics of the blood flow, the trans-valvular pan-cyclic gradients, and the high shear stress and mal-coaptation of cusps.5 These processes promote fusion of cusps, valve degeneration and remodeling of the aortic wall, which progress to AR.6–8 These functional and anatomical changes develop over time and approximately 15% of patients will eventually develop moderate-severe AR,4 which can negatively affect the “stability” of LVAD therapy. The volume of aortic regurgitation prevents an adequate discharge of the left ventricle and causes an increase in the end-diastolic pressure. In addition, anterograde cardiac output is compromised by a continuous cycle situation in which blood circulates through the LVAD into the aorta, but is then regurgitated into the left ventricle through the aortic valve, then anterograde through the LVAD, and so on. If the volume of regurgitation is large enough, symptoms of heart failure can develop. At this point, it is necessary to take into account a modulation of the speed of the LVAD, an intervention on the aortic valve or eventually an urgent heart transplant.9
A review of pulmonary autograft external support in the Ross procedure
Published in Expert Review of Medical Devices, 2019
Vincent Chauvette, Marie-Ève Chamberland, Ismail El-Hamamsy
Dilatation of the pulmonary autograft is one of the most feared complication of the Ross procedure. Its occurrence is associated with the development of aortic regurgitation and the need for reoperation. Effort to minimize the risks of pulmonary autograft dilatation should be actively pursued in order to maximize the benefits associated with the Ross procedure. Providing external support to the autograft effectively prevents dilatation. However, it might also hamper aortic root hemodynamics and have deleterious effects on coronary perfusion. The use of prosthetic material might also be concerning for the risk of endocarditis. Temporary external support with the use of bioengineered materials is a promising approach; combining the advantages of early external support with the long-term benefits of normal root hemodynamics. Further research in this field is needed to determine the long-term outcomes of these techniques and to further develop treatments aimed at mitigating the risks of pulmonary autograft dilatation.
Pre-implantation genetic testing for Marfan syndrome using mini-sequencing
Published in Journal of Obstetrics and Gynaecology, 2022
Sirivipa Piyamongkol, Krit Makonkawkeyoon, Vorasuk Shotelersuk, Opas Sreshthaputra, Tawiwan Pantasri, Rekwan Sittiwangkul, Theera Tongsong, Wirawit Piyamongkol
Marfan syndrome (MFS1, OMIM#154700) is the most common connective tissue disorder. MFS1 is inherited in an autosome dominant manner. Its incidence is about 2–3 in 10,000. It was first clinically described in 1896 (Marfan 1896). Major phenotypes include skeletal, ocular and cardiovascular system involvement. Anterior chest and vertebral column deformity, disproportionately tall stature, arachnodactyly and joint laxity are common skeletal manifestations. Ectopia lentis is a key ocular characteristic. Cardiovascular manifestations are the leading cause of the morbidity and mortality associated with Marfan syndrome. Aortopathy, i.e. aortic root dilatation, aortic regurgitation secondary from aortic dilatation, and fatal aortic dissection are the major causes. A family history of aortic dissection is the most important predicting factor for the risk of aortic dissection in affected offspring (Pyeritz 1993).
Related Knowledge Centers
- Aorta
- Aortic Valve
- Paroxysmal Nocturnal Dyspnoea
- Shortness of Breath
- Diastole
- Ventricle
- Heart
- Orthopnea
- Heart Failure
- Signs & Symptoms
- Shortness of Breath