Hypertension: There are three major things central to hypertension. They include increased systemic vascular resistance, increased vascular stiffness and increased vascular responsiveness to stimuli.

Hypertrophy: Cells increase in size to deal with increased workload. With increased vascular resistance and vascular stiffness in the circulation distal to the heart (aka increased cardiac afterload), the heart cells in the left ventricle get bigger, leading to LVH.

LVH is a relatively early response to hypertension; it is even demonstrated on echocardiogram of children and adolescents with borderline hypertension. LVH may even begin before hypertension because the same factors (angiotensin II, norepinephrine, epinephrine, increased sympathetic drive, and endothelin) promoting both HTN and LVH .

Why is LVH a problem?

•  LVH is an increased in muscle mass and wall thickness but not ventricular volume. It also leads to decreased elasticity of the heart muscle.
• It impairs diastolic function, slows relaxation and delays filling.
• It can lead to chronic pressure overload which leads to heart failure
• Complications can occur such as arrhythmia, ischemia, MI, and sudden cardiac arrest. These complications are likely due to two things. First, there is reduced density of capillaries in hypertrophied myocardium. Second, the enlarged muscle mass limits the ability of the coronary arteries to dilate and respond to decreased perfusion.
• The perfusion issues that we have just discussed can make the heart irritable and at risk of arrhythmia but there is also some remodeling of the electrical system of the heart in LVH. This could include prolongation of the action potential (i.e. leading to bundle branch block), altered repolarization and early action potentials (leading to VF, VT, torsades, or atrial fibrillation). 

• Shortness of breath
• Chest pain
• Palpitations
• Dizziness and fainting spells
• Quick exhaustion with physical activity.

1. Which organism is most frequently found in drug addicts with infective endocarditis?
Answer: Staphyloccus aureus is the most frequent organism found in drug addicts along with other skin contaminants.

2. What is the most frequent final outcome of this disease in drug addicts with antibiotic treatment and valve replacement?
Answer: There is a very high mortality rate in drug addicts that develop acute bacterial endocarditis despite antibiotic treatment and valve replacement.

3. Give cardiac and extracardiac complications of infective endocarditis?
Answer: The complications of infective endocarditis include cardiac failure, disseminated infection, systemic embolization (which can secondarily cause myocardial, splenic, cerebral, renal infaction) and cardiac arrythmias.

4. What is the minimum number of blood cultures required to arrive at a definitive diagnosis?
Answer: The recommendation is at least 2 blood cultures, 15-60 minutes apart for a given febrile episode.

5. Compare marantic with infective endocarditis, clinically and histologically.
Answer: The vegetations seen in marantic (nonbacterial thrombotic) exhibit small bland vegetations, usually attached at the line of closure of the valve leaflets. They consist of fibrin and platelets with no inflammation or microorganisms. They are seen in association with malignancy or other debilitating disease and generally occur on normal cardiac valves. The vegetations in infective endocarditis are large irregular masses on the valve cusps that can extend onto the cords. They consist of fibrin, platelets, inflamatory cells and bacteria. They can present clinically as acute or subacute endocarditis. They can occur on normal or abnormal cardiac valves, the former being more characteristic of acute endocarditis