Alpert Valvular Heart Disease

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Structural heart disease is congenital or acquired pathologies outside of atherosclerosis. The growth of percutaneous therapies for the treatment of structural heart disease has led to the need to train high-quality physicians with expertise in these diseases and procedures. The Interventional Structural Heart Disease Fellowship at Brown is a 1 year, non-ACGME, program designed for fellows that desire further training in structural heart disease, non-coronary interventions, and high risk percutaneous coronary intervention. The experience includes clinical, diagnostic, and catheter-based therapy. To be eligible, fellows must complete an ACGME approved 1 year training program in Interventional Cardiology.

The purpose of the training program in interventional structural heart disease is to prepare fellows to care for patients with acquired or congenital cardiovascular pathologies that involve the major central cardiovascular structures outside of the acquired atherosclerotic coronary and peripheral vascular pathologies. The program also includes a research component.

Young women may have asymptomatic mitral valve disease which becomes unmasked during the haemodynamic stress of pregnancy. Rheumatic mitral stenosis is the most common cardiac disease found in women during pregnancy. The typical increased volume and heart rate of pregnancy are not well tolerated in patients with more than mild stenosis. Maternal complications of atrial fibrillation and congestive heart failure can occur, and are increased in patients with poor functional class and severe pulmonary artery hypertension. Patients can be diagnosed by echocardiography and symptoms treated with beta-1 antagonists and cautious diuresis. Patients with heart failure unresponsive to treatment can undergo percutaneous balloon mitral valvuloplasty. Labour and delivery goals include reducing tachycardia by adequate pain control and minimized volume shifts. Mitral valve regurgitation, even when severe, is usually very well tolerated in pregnancy as the increase in volume is offset by a decrease in vascular resistance. On the other hand, patients with left ventricular dysfunction, moderate pulmonary hypertension or NYHA functional class III-IV are at increased risk for heart failure and arrhythmias. They may need cautious diuresis and limitations on physical activity during pregnancy, as well as invasive haemodynamic monitoring for labour and delivery. Vaginal delivery is preferred and caesarean section reserved for obstetric indications.

Valvular and perivalvular involvement in end-stage renal disease (ESRD) is most commonly manifested as mitral annular calcification and aortic valve calcification. Both mitral and aortic valve calcification (MAC) occur more frequently and at younger age in those with ESRD than in those with normal renal function. Aortic valve calcification progresses to aortic stenosis more commonly and at a more accelerated rate than in the general population. Altered calcium and phosphate metabolism are thought to predispose to these valvular and perivalvular abnormalities. No treatment is necessary for MAC unless severe mitral regurgitation or stenosis occur (both are rare). Mitral valve repair or replacement and aortic valve replacement are indicated for severe symptomatic valve stenosis or regurgitation, albeit at a higher risk than in those with normal renal function. Infective endocarditis may complicate MAC or aortic stenosis in patients with ESRD and is associated with a high mortality rate in such patients.

A similar situation exists in the cardiovascular system. Deformity of valvular structures, valvular stenosis, and discontinuity in a wall of the heart or in the great vessels may provide a site for vortex shedding. Moreover, substantial vortex shedding can result from increased flow over the normal protrusions and irregularities in the heart or great vessels. The response of blood moving to fill the wakes left by the shedding of vortices is an efficient mechanism for the generation of sound and is capable of giving rise to sustained vibrations that are audible at the chest wall (i.e., murmurs).

Systolic murmurs may be further subclassified as functional or organic. Functional systolic murmurs occur in the absence of cardiac structural abnormalities. They are frequently encountered in healthy individuals, but may also accompany a variety of high cardiac output states. Organic systolic murmurs evolve from structural abnormalities in the heart or great vessels. Systolic ejection murmurs may be functional or organic, but systolic regurgitant murmurs indicate organic heart disease.

Aortic sclerosis results from degeneration and calcification of the aortic cusps, predominantly at their base. This abnormality produces a murmur that is identical in character to aortic valvular stenosis but does not result in a pressure gradient over the aortic valve. The murmur typically peaks in midsystole and is accompanied by a normal second heart sound and carotid pulse upstroke. The responses to physiologic and pharmacologic interventions are identical to those of functional systolic ejection murmurs. Echocardiographic studies suggest that aortic sclerosis is common in the elderly and may be the single most common cause of systolic murmur in this population.

The murmur of rheumatic mitral valve regurgitation is high pitched, blowing, and best heard at the cardiac apex with radiation to the axilla. It is holosystolic, starting with the first heart sound and extending to and sometimes through the aortic component of the second heart sound. Typically plateau in configuration, the murmur occasionally has late systolic accentuation. The intensity of classic mitral valve regurgitation is quite variable. The intensity increases with squatting, isometric hand grip exercise, and intravenous administration of alpha-adrenergic agonists. It typically decreases with amyl nitrite inhalation. As a result of the volume overload state associated with valvular mitral regurgitation, a third heart sound is commonly audible at the apex. Dilated cardiomyopathy can produce a mitral regurgitation murmur similar in character to rheumatic mitral valve regurgitation.

Acute mitral valve regurgitation is most commonly caused by chordae tendineae rupture, but may also result from papillary muscle rupture, infective endocarditis, or trauma. The murmur of acute mitral regurgitation is typically decrescendo and of variable intensity (usually grade 3 or higher). It begins with the first heart sound and decreases in intensity throughout systole, occasionally terminating before the aortic component of the second heart sound. Best heard at the cardiac apex, the murmur typically radiates to the axilla and may be audible along the cervical spine or at the top of the head in selected cases. The murmur is lower pitched than that of rheumatic mitral regurgitation, often possessing a harsh quality reminiscent of valvular aortic stenosis. A third and fourth heart sound may be audible at the apex.

Dr. Thaden has an active clinical practice including clinical activities at Mayo Clinic in Rochester, Minnesota, and the Red Wing Medical Center in Red Wing, Minnesota. In addition to his clinical activities, he is active in research, where he focuses on valvular heart disease and the application of existing and novel echocardiographic techniques to improve patient care.

Cardiology is the branch of medicine that specializes in the study, diagnosis, and management of pathologies affecting the heart. Dysfunction of the cardiac pump can manifest in several ways depending on the underlying cause. Respiratory signs and symptoms are common in the case of poor cardiac performance or inadequate oxygenation of blood.In this course, the student will be given overview of heart failure, congenital heart diseases, valvular diseases, coronary artery disease, the different types of cardiomyopathies, cardiac dysrhythmias, and hypertension. For optimal understanding, the student should be familiar with the anatomy of the heart, with special emphasis on coronary circulation and the conduction system, and cardiac physiology, with special attention to the cardiac cycle and membrane potential.

SPVR still remains the gold standard for patients with congenital heart diseases. TPVR can be a reliable and safe alternative to SPVR in patients that have undergone prior surgeries for congenital heart disease. A careful anatomic and hemodynamic assessment is essential to select appropriate candidates for this procedure.

Background: Early diagnosis and improved facilities are necessary for determining the optimal timing of surgery and other interventions in children with congenital heart diseases in Nigeria. This is because late presentation, late diagnosis and delayed surgery can lead to mortality and affect the quality of life among these children.

Congenital heart disease is becoming a common cause of congenital abnormalities in our locale [1]. There is also a dramatic increase of the prevalence of congenital heart disease (CHD) which has risen from 4 to 5 per 1,000 live births among older studies to 12 to 14 per 1,000 live births, reported in the recent literature [2]. In the foregoing therefore, the diagnosis and treatment for congenital cardiac disease has also undergone remarkable progress over the last 6 decades [3]. Accurate timing and intervention significantly improves quality of life, prevents complications and reduces the morbidity and mortality associated with these defects. Worldwide, CHD are the main cardiac anomaly found in children and constitute one of the major causes of infant mortality, particularly in developing countries [4].

The indications and timing of intervention among children with congenital heart disease is decided by the severity and type of the lesion. For instance, balloon pulmonary valvuloplasty is the treatment of choice for valvar pulmonary stenosis and surgery must be done when the peak-to-peak systolic pressure gradient is more than 50 mmHg across the pulmonary valve [5]. For aortic valve stenosis, balloon aortic valvuloplasty appears to be the first therapeutic procedure of choice with intervention feasible when peak-to-peak systolic pressure gradient across the aortic valve in excess of 70 mmHg irrespective of the symptoms or a gradient more than and equal to 50 mmHg with either symptoms or electrocardiographic ST-T wave changes indicative of myocardial perfusion abnormality [6]. The indications for intervention in coarctation of the aorta are significant hypertension and/or congestive heart failure along with a pressure gradient in excess of 20 mmHg across the coarctation [7]. In addition, it is important to remember that the defect once detected should be corrected whether by surgery or by nonsurgical methods as appropriate before ventricular dysfunction, pulmonary vascular change and other complications ensue. 2b1af7f3a8