Cardiovascular pathology 1 Flashcards
ISCHAEMIC HEART DISEASE definition
Generic designation for a group of syndromes resulting from myocardial ischaemia
(An imbalance between demand and supply of oxygenated blood to the heart)
IHD epidemiology
435 people die a day due to cardiovascular disease, 12 babies born a day with heart defect. Prevalence of IHD is highest in Northern England and Scotland.
IHD Aetiology:
Almost always caused by coronary artery atherosclerosis. Sometimes due to hypertrophy (demand)
Myocardial Infarction: Duration and severity of ischaemia causes myocardial death
Angina Pectoris: Ischaemia is less severe and does not cause myocardial death (Stable angina = typical /Prinzmetal angina= variant angina /Unstable angina) – Acute coronary syndrome = MI, unstable angina an chronic IHD
Chronic IHD with heart failure, Sudden cardiac death (4 ischemic heart disease syndromes)
IHD risk factors
High blood pressure; Lipid profile abnormalities and Diabetes, Not total cholesterol but high HDL and a low TC:HDL ratio which are better indicators of risk for CVD, Smoking and a sedentary lifestyle
IHD Pathogenesis
Myocardial ischemia is a consequence of reduced blood flow in coronary arteries, due to a combination of fixed vessel narrowing and abnormal vascular tone as a result of atherosclerosis and endothelial dysfunction. This leads to an imbalance between myocardial oxygen supply and demand. Ischemia takes place after 75% of coronary vessel is occluded.
MYOCARDIAL INFARCTION
Death of cardiac muscle from prolonged ischemia.
Transmural vs Subendocardial. Inner 1/3rd of heart wall is most vulnerable part of heart wall).
Pathophysiology: Acute plaque changes, Platelet aggregation, Thrombus formation, Occlusion of coronary artery
Complications: Arrhythmias – either directly or by limited perfusion to the conduction system structures (SA node, etc), Congestive cardiac failure – contractility dysfunction or by papillary muscle infarct/severe MR, Thromboembolism, Pericarditis, Ventricular aneurysm, Cardiac tamponade (full thickness of myocardium is infarcted), cardiogenic tamponade.
Clinical features of MI
Blood markers of IHD
Troponins T & I: detectable 2 – 3h, peaks at 12h, detectable to 7 days. Raised post MI but also in pulmonary embolism, heart failure, & myocarditis. Proteins released by damaged myocytes.
Creatine kinase MB: detectable 2 – 3h, peaks at 10-24h, detectable to 3 days. Enzyme found in brain, skeletal muscles and heart.
Myoglobin: peak at 2h but also released from damaged skeletal muscle
Lactate dehydrogenase isoenzyme 1: peaks at 3days, detectable to 14days
Aspartate transaminase; Also present in liver so less useful as a marker of myocardial damage
Hypertensive heart disease
Cause: Arteries are constricted or directly blocked or disorders affecting chest movement eg obesity
Systemic (left sided) hypertensive heart disease
In hypertension, hypertrophy of the heart is an adaptive response to pressure overload that can lead to myocardial dilation, congestive heart failure and sudden death.
Criteria: Left ventricular concentric hypertrophy, History or pathological evidence for hypertension
Pulmonary (right sided)
hypertensive heart disease (cor pulmonale)
Right ventricular hypertrophy, dilation and potentially heart failure secondary to pulmonary artery hypertension caused by disorders of the lung or pulmonary vasculature.
Right ventricular hypertrophy secondary to diseases of the left side and congenital causes are generally excluded in the definition; but pulmonary venous hypertension that follows left sided diseases is quite common.
Systemic hypertension
Definition: Blood pressure (BP) is considered to be a continuously distributed variable, and essential hypertension is one extreme of this distribution rather than a distinct disease.
The detrimental effects of raised BP increase continuously as pressure rises.
A sustained diastolic pressure greater than 90 mm Hg or sustained systolic pressure greater than 140 mm Hg.
Primary systemic hypertension
Aetiology: The majority of patients (90%) have primary essential hypertension of unknown cause.
Epidemiology: the prevalence of hypertension in adults of 16 years or older was 31.5% in men and 29.0% in women
WHO estimated over 1 billion people worldwide in 2008, Vulnerability to complications increases with age, Africans affected more.
Aetiology: The critical roles of cardiac output and peripheral resistance in blood pressure regulation
The renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating blood volume and systemic vascular resistance, which together influence cardiac output and arterial pressure.
Secondary hypertension
Accounts for 5% of hypertension patients
Cushing’s – Cortisol – stimulates the sympathetic nervous system and has an aldosterone like action on the kidneys
Conn’s disease – Aldosterone – Na+ and water retention = hypertension
Pheochromocytoma – Catecholamines – Adrenaline and Noradrenaline
Coarctation – congenital narrowing of the aorta
Renal artery stenosis- juxtaglomerular apparatus stimulated to produce renin
Malignant Hypertension:
BP >180/120mmHg
Clinically signs & symptoms of organ damage
acute hypertensive encephalopathy and/or nephropathy with retinal haemorrhages/papilloedema
Requires urgent treatment to preserve organ function
ANEURYSMS
Definition: A localised abnormal dilation of a blood vessel or the wall of the heart.
True aneurysm – when bounded by arterial wall components or the attenuated wall of the heart.
False aneurysm – (pseudoaneurysm) is a breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space (“pulsating hematoma”)
