The cardiovascular system can fail for many different reasons. Firstly, there might be an issue with the heart pump itself: it might not contract enough or relax enough. Secondly, there may be issues with flow: flow may be obstructed (due to a plaque etc.), regurgitant (due to a leaky heart valve), or shunted (diverted due to a congenital or acquired heart defect). Thirdly, there may be issues with conduction of the electrical signal, leading to problems with contraction of the heart.
Causes, consequences and pathological findings of cardiac hypertrophy
The heart may hypertrophy due to an overload in pressure or an overload in volume. An overload in pressure will result in addition of new myofibrils, leading to thickening of the heart wall. This is known as concentric hypertrophy. On the other hand, increased volume will lead to the addition of new sarcomeres, causing the heart chambers to become larger. This is known as eccentric hypertrophy. Cardiac hypertrophy may also be accompanied by synthesis of abnormal protein and DNA, fibrosis (due to the blood supply being insufficient for a larger heart), or other molecular changes.
Causes and clinical manifestations of heart failure
Heart failure, as discussed here, is when the cardiac output fails to meet the needs of the body. Heart failure can be classified in many different ways.
- Forward vs. backward: In forward heart failure, not enough blood leaves the heart. In backward heart failure, heart backs up into the venous system.
- Left vs. right: Kind of self-explanatory- simply refers to the side of the heart affected.
- Systolic vs. diastolic: In systolic heart failure, there is inability to contract normally. In diastolic failure, there is inability to relax and fill properly. (Note: systolic heart failure is sometimes also known as heart failure with reduced ejection fraction, or HFrEF, and diastolic heart failure is also known as heart failure with preserved ejection fraction, or HFpEF.)
- High vs. low output: In high output heart failure, the heart is pumping out a lot of blood, but due to increased demand by the body, this is still insufficient to supply the body. In low output heart failure, there is insufficient output of blood.
- Acute vs. chronic: Acute onset is sudden (perhaps due to a sudden myocardial infarction), and chronic occurs over time.
There are a range of different clinical manifestations that may accompany heart failure. I have discussed them here.
Pathological findings of hypertensive heart disease, including pulmonary hypertension
Hypertensive heart disease is characterised by left ventricular hypertrophy (thickness of over 15mm and heart weight greater than 500g) with a history of hypertension, but no other cardiovascular pathology. Since the ventricle wall is thick, diastolic filling is impaired. The atria may also hypertrophy in order to try and force blood into the ventricle. Sudden death may result from hypertensive heart disease.
Pulmonary hypertension is essentially the right-sided heart's answer to systemic hypertensive heart disease. It is defined by a pulmonary arterial pressure greater than 30mmHg or greater than 25% of systolic pressure. Pulmonary hypertension can cause right ventricular enlargement, or cor pulmonale.
Aetiology, pathogenesis, classification, morphological changes, clinical features and clinical sequelae of ischaemic heart disease
Aetiology and Pathogenesis
Ischaemic heart disease usually results from atherosclerosis. Therefore, aetiological factors of ischaemic heart disease are basically the same as those for atherosclerosis: see here.
Classification
The four main types of ischaemic heart disease are angina pectoris, myocardial infarction, chronic ischaemic heart disease with heart failure, and sudden cardiac death.
Morphological changes, clinical features, and clinical sequelae
Angina pectoris can be further broken down into three types: stable, Prinzmetal (or variant), and unstable. I have discussed them here.
Myocardial infarctions can be transmural, meaning that they affect the whole thickness of the wall, or subendocardial, meaning that they only affect part of the wall. The damage in myocardial infarction usually starts from the subendocardial area and extends outwards. I have discussed myocardial infarction here.
Chronic ischaemic heart disease with heart failure is progressive and involves a widespread narrowing of coronary arteries. There may be widespread fibrosis and endocardial thickening.
Sudden cardiac death is basically what it says on the box. In this case, "sudden" is defined as being death within 1-24 hours of the onset of symptoms. It is thought to be due to some kind of arrhythmia.
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