Ciara Gavin MPSI looks at the clinical considerations in cardiology and some of the more prevalent conditions in cardiovascular disease
Introduction
The heart is the largest muscle in the body and has a primary function of circulation. With each beat, the heart pumps blood around the body, transporting oxygen to the organs which is necessary for them to function. Cardiovascular disease (CVD) is the most common cause of death in Ireland, accounting for approximately 36 per cent of deaths.1
Prevention of cardiovascular disease is extremely important. The elimination of the health risks linked to cardiovascular disease is estimated to prevent 80 per cent of cases of CVD. Modifiable health risks include: High blood pressure, obesity, high blood cholesterol, insufficient physical activity, diabetes, and excess alcohol consumption. Cardiovascular risk can be assessed using SCORE or a similar assessment tool.2,3
CVD encompasses conditions affecting the heart or the blood vessels. CVD includes coronary heart disease (CHD), stroke and peripheral arterial disease. These are also linked to conditions such as heart failure and chronic kidney disease.4
Heart Failure
Heart failure is a condition where the heart is unable to generate a cardiac output sufficient for the body and the heart becomes too weak to pump the blood around the body.5 It is a clinical syndrome which is characterised by common symptoms such as shortness of breath, difficulty breathing, ankle-swelling or fatigue. Common causes of heart failure include CAD, HTN, valvular disease and myocarditis.5
Heart failure can be categorised as those with normal left ventricular ejection fraction: LVEF (>50%); preserved ejection fraction; and those with reduced ejection fraction (<40%). Heart failure with an ejection fraction of between 40-to-49 per cent has recently been reclassified as a mid-range ejection fraction, HFmrEF. Differentiation of patients based on the LVEF is important due to different aetiologies and response to therapy.5
Classification tools are commonly used to describe the severity of symptoms and the exercise intolerance of patients — an example of this is the New York Heart Association (NYHA).6 The classification ranges from patients’ symptoms: (i) No limitations of physical activity, to (iv), inability to carry out any physical activity and symptoms of heart failure at rest. Objective classification ranges from A to D, with (A) being no objective evidence of cardiovascular disease, to (D), evidence of severe cardiovascular disease.6
Heart failure can present acutely as a consequence of a trauma, ie, an acute myocardial event, or in a gradual fashion, ie, in patients with a dilated cardiomyopathy.5 In most cases, signs and symptoms may resolve with treatment, however the cardiac dysfunction will not and the patient will remain at risk of decompensation or recurrence.5 In some less-frequent cases, patients with heart failure due to a specific problem, ie, viral myocarditis, can completely resolve.5
Congestive heart failure is often used to describe acute or chronic heart failure where signs or symptoms of fluid overload are present, such as shortness of breath.5
Diagnosing heart failure is completed using a variety of tests. Some examples of such are:
Blood tests: Natriuretic peptide (NP) levels (B-type natriuretic peptide — BNPs) are markers used to identify if further investigation is required. If raised, they are indicative for a heart failure diagnosis once further testing is completed. Currently, these are used to help rule-out heart failure, but not yet to diagnose.5,7
ECG: An abnormal ECG increases the likelihood of HF, however this is unspecific, as many indications can cause an abnormal ECG, however if a patient presents with a completely normal ECG, this is then unlikely to be HF.5
Echocardiography: Echo is the most useful test for heart failure. This provides information on chamber volume, ventricular systolic and diastolic function, wall thickness, valve function and pulmonary hypertension.5
Treatment aims for heart failure include: To improve symptoms, quality of life, prevent hospital admissions, and reduce mortality.5
Some treatment options
Patients who present with signs and symptoms of overload will be treated with diuretics such as furosemide to remove excess fluid and improve symptoms. However, the cornerstone of heart failure treatment are ACE-I/ARBs and beta-blockers. ACE-I have been shown to reduce mortality and morbidity in patients with HF. Treatment should be up-titrated to the maximum tolerated dose. ARBs show improved exercise tolerance and improved quality of life.5 Some trials have shown ACE-I to reduce hospitalisations.8 Patients will be on either an ACE-I or an ARB, but not both due to risks of hyperkalaemia.5
Beta-blockers may be added to ACE-I therapy. They can cause regression of LV hypertrophy, reversal of adverse remodelling and improved LV relaxation and distensibility. Beta-blocker therapy is recommended in patients with previous MIs, HTN and AF.5
Mineralocorticoid/aldosterone receptor antagonists: Spironolactone or eplerenone are recommended in all symptomatic patients, despite treatment with an ACE-I or beta-blocker with HFrEF and LVEF <35%, to reduce mortality and hospitalisation.9
Hypertension
Hypertension is a major risk factor for cardiovascular disease and is linked to many other diseases; it is a leading risk factor for disease burden globally. The prevalence for hypertension is ~30-to-45 per cent in adults over the age of 18.2,10
The risk of death from CAD or stroke increases progressively and linearly from BP levels as low as 115/75 upwards. Normal blood pressure is considered readings of systolic (SBP) 120-to-129 and/or diastolic (DBP) 80-to-84, high-normal (SBP) 130-to-139 and/or (DBP) 85-to-89, and anything above this is considered hypertension.2,10 The European Society of Cardiology further breaks down the readings to:
Grade 1 hypertension (SBP) 140-to-159 and/or (DBP) 90-to-99;
Grade 2 hypertension (SBP) 160-to-179 and/or (DBP) 100-to-109;
Grade 3 hypertension (SBP) >180 and/or >110 (DBP).
Treatment options
Lifestyle changes are recommended in all patients with hypertension. The decision to start antihypertensive therapy will depend on the patient’s BP and cardiovascular risk score. Combination treatment is needed to control blood pressure in the majority of patients.
Thiazide and thiazide-like diuretics, beta-blockers, calcium channel blockers, ACE-inhibitors and ARBs can all control BP and reduce the risk of cardiovascular death and morbidity. Therefore, these medications are all recommended for the initiation and maintenance of blood pressure control, either as monotherapy or combination therapy.10
Medications with 24-hour control are preferred agents to aid adherence. Consideration of patient comorbidities and additional benefits should be made when considering choice of therapy. For example, ACE and ARBs are effective in reducing LVH, reducing micro-albuminuria and proteinuria-preserving renal function, and delaying end-stage renal disease.10
Atrial Fibrillation linked to stroke
One-in-four middle-aged adults in Europe and the US will develop atrial fibrillation (AF). It has a greater prevalence in patients with conditions such as hypertension, heart failure, coronary artery disease, obesity, diabetes, CKD, and valvular heart disease.11
It is estimated that between 20-to-30 per cent of all strokes are due to AF. Death due to stroke can be mitigated against by using anticoagulation. Oral anticoagulation with warfarin or a non-vitamin k antagonist (NOAC) reduces the risk of stroke and reduces mortality. It is recommended that anticoagulants be used in most patients with AF unless contraindicated.11
To identify the stroke risk, patients should be assessed using the CHA2DS2-VASc score and risk of bleed using the HASBLED score, which can identify patients requiring anticoagulation. Patients with a CHA2DS2-VASc score of 1 or more in men and 2 or more in women would benefit from oral anticoagulants.11
The preferred NOAC currently in Ireland is apixaban, per the HSE medicines management programme (MMP). The following published trials, RE-LY, ROCKET-AF, ARISTOTLE and ENGAGE AF-TIMI 48 provide useful information on the risks and benefits of the different NOAC options for AF.11
Patients can present on combination therapy of oral anticoagulants and antiplatelets. This can be due to the consideration that approximately 15 per cent of AF patients have a history of MIs and a portion will require stenting in their lives. A clinical decision will be made balancing the risk of bleed, stroke risk and risk of ACS.11
Prescribing dual antiplatelet (DAPT) and oral anticoagulants increases the risk of major haemorrhage. The addition of a NOAC increased bleeding risk by 79-to-134 per cent, while reducing recurrent ischaemic events only marginally in patients without AF. Therefore, NOAC monotherapy is preferred in patients with AF and stable CAD without ACS or coronary interventions in the previous 12 months. In patients treated for ACS, and in those receiving a coronary stent, short-term therapy of DAPT plus NOAC seems warranted. AF patients at risk of stroke, patients with mechanical valves and patients with recent or recurrent DVTs or PEs are generally advised to continue NOACs during and after stenting. A short period of triple therapy is recommended for these patients, followed by a period of NOAC plus single antiplatelet agents. In these patients, it is advisable to use aspirin plus clopidogrel as the DAPT due to a lack of evidence and greater bleeding risks associated with alternative antiplatelet therapies.11
