CARDIAC HYPERTROPHY

“His heart grew three sizes that day”



Cardiac Hypertrophy is the adaptive growth of heart muscle. Just like your biceps, the heart can grow larger if it has to do more work. This commonly occurs with hydrostatic stress (high pressure from hypertension, for example) or with a high sympathetic tone. This is a normal, healthy response . . . at first. If the heart grows too large, it loses efficacy, and heart failure ensues. When cardiac hypertrophy turns harmful, we refer to it as cardiomyopathy. A fundamental problem with cardiomyopathy is that the muscle growth is not accompanied by a proportional growth in capillaries, which makes the enlarged heart more vulnerable to ischemia, CHF and death.


There are two different kinds of cardiac hypertrophy: Hypertrophic and Dilated. 


CARDIOMYOPATHY

Heart muscle disease



DILATED CARDIOMYOPATHY is the dilation of the chambers. The walls stretch out and become floppy and weak. CO plummets. This is systolic heart failure. Stretching of the valves can result in regurgitant valves. Stretching of the myocytes can result in arrhythmias. It’s most commonly idiopathic; other causes include genetic mutations (AD mutation of Titin protein), myocarditis (Coxsackie / Chagas), alcoholism, wet beriberi (B1 deficiency), drugs (Doxorubicin, cocaine) and pregnancy. There isn’t a good treatment. An LVAD device can hold you over until a heart transplant. On EKG, the QRS spikes will be tall (more muscle)


HYPERTROPHIC CARDIOMYOPATHY is the growth of the walls. The huge muscle protrudes into the LV chamber, limiting diastolic filling. The beefy wall also loses flexibility and compliance. This decreases LV end diastolic volume (LVEDV), thus limiting CO. This is diastolic heart failure. Most commonly due to AD genetic mutations in myosin proteins, hypertension and Friedreich's Ataxia. 


There is another condition called HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY where the muscle growth is limited to the interventricular septum. This is a problem because contraction makes the muscle widen further, and it can obstruct the Aortic valve. The heart beats faster and harder during exercise, which leads to symptom flares with exercise. Symptoms are due to the drop in CO to the brain, namely syncope. This is a genetic condition, it is often diagnosed in teenage athletes. Unfortunately, the terminology around this is frustrating. Many call it simply “Hypertrophic Cardiomyopathy.” On biopsy, there will be myofiber hypertrophy and disarray. There is a murmur that is similar to Aortic Stenosis. But there’s a big difference. If you increase LV volume (handgrip increases afterload, leg raise increases preload), the thiqq septum will be pushed apart from the LV outlet, quieting the HOCM murmur. In Aortic Stenosis, more LV volume means more blood will whoosh past the stenotic valve, making the murmur louder.



HOCM

Restrictive Cardiomyopathy is the decreased compliance of the ventricles. The stiff ventricles cannot fill with blood during diastole. Caused by the deposition of biomolecular trash into the myocardium: amyloid protein (Amyloidosis), granulomas (Sarcoidosis), iron (Hemochromatosis) or eosinophilic fibrosis in the myocardium (Löffler Syndrome). They will present as diastolic CHF, but two signs differentiate them from Hypertrophic Cardiomyopathy: auscultation reveals a cardiac knock (which sounds just like an S3 sound) and small QRS spikes on EKG. 





HEART FAILURE

Low cardiac output



Heart Failure refers to a heart that pumps poorly. Across the bajillion different categorizations, there is the consistent element: low cardiac output. 


Timing of CHF

Most of the time CHF is asymptomatic. Patients live fairly normal lives, aside from exercise intolerance. Their CO is low, and their hearts are stressed out, but their body can compensate (RAAS, SNS). But sometimes CHF flares up. Flare ups are usually caused by excessive sodium intake -- the body is great at absorbing salt, but very bad at getting rid of it. To normalize the sodium concentration, the body retains some extra water (using ADH). Healthy patients can distribute that extra water evenly across their entire circulatory system. But with heart failure, the fluid gets backed up behind the shoddy pump (heart). That extra water (hypervolemia) causes all of the classic symptoms of heart failure. Symptoms occur “upstream” from the failing heart. This will hopefully become clear over the next few pages.



Diagnosis of CHF

The gold standard is the clinical gestalt of a cardiologist. Other tests include an elevated BNP (Brain Natriuretic Peptide) and an abnormal Echo (you don’t have to interpret Echos).


Categories of CHF

There are two ways to think about CHF classification. 




SYSTOLIC Heart Failure


The heart muscle is weak. Part of the heart wall dies, leaving an inert scar. The Ejection Fraction is low (<45%), AND the stroke volume is low. Most common cause: MI. Next most common cause is dilated cardiomyopathy.

DIASTOLIC Heart Failure 


The heart can pump, but it can’t refill. As the heart muscle becomes beefier, it loses compliance and starts growing into the chamber, leaving less room for blood.  Look at this thiccy. The Ejection Fraction is normal (45 - 65%), but the stroke volume is low. Most common cause: Hypertension

Right Heart Failure

Less common. If due to lung disease (pulmonary hypertension) it’s called cor pulmonale



Left Heart Failure

Left CHF causes lung symptoms at first, then it will cause Right CHF.

Note - most cases of real-world cases of CHF involve both sides



CHF TREATMENT


Acute CHF Treatment -- the goal is to remove fluid. Diuretics put fluid into pee, Nitrates allow more room for fluid in veins.



Chronic CHF Treatment - The goal is to prevent the heart from (a) undergoing further pathological cardiomyopathy or (b) prevent further cardiac ischemia. Since cardiomyopathy is driven by a high sympathetic and RAAS tone, drugs that lower sympathetic and RAAS tone are the most effective at preventing further tissue growth.