Myocardial infarction (MI) is a serious condition that requires proper management to prevent further complications. In 2013, NICE released guidelines on the secondary prevention of MI. One of the key recommendations is the use of four drugs: dual antiplatelet therapy (aspirin plus a second antiplatelet agent), ACE inhibitor, beta-blocker, and statin. Patients are also advised to adopt a Mediterranean-style diet and engage in regular exercise. Sexual activity may resume four weeks after an uncomplicated MI, and PDE5 inhibitors may be used six months after the event.

Most patients with acute coronary syndrome are now given dual antiplatelet therapy, with ticagrelor and prasugrel being the preferred options. The treatment period for these drugs is 12 months, after which they should be stopped. However, this period may be adjusted for patients at high risk of bleeding or further ischaemic events. Additionally, patients with heart failure and left ventricular systolic dysfunction should be treated with an aldosterone antagonist within 3-14 days of the MI, preferably after ACE inhibitor therapy.

Overall, the NICE guidelines provide a comprehensive approach to the secondary prevention of MI. By following these recommendations, patients can reduce their risk of further complications and improve their overall health outcomes.

Long QT syndrome can be caused by hypokalaemia, which is an electrolyte imbalance that leads to a prolonged corrected QT interval on an ECG. This condition is often seen in young people and can present as cardiac syncope, tachyarrhythmias, palpitations, or cardiac arrest. Long QT syndrome can be inherited or acquired, with hypokalaemia being one of the acquired causes. Other causes include medications, CNS lesions, malnutrition, and hypothermia. It’s important to note that hypercalcaemia is associated with a shortened QT interval, not a prolonged one.

Understanding Long QT Syndrome

Long QT syndrome (LQTS) is a genetic condition that causes delayed repolarization of the ventricles, which can lead to ventricular tachycardia and sudden death. The most common types of LQTS are caused by defects in the alpha subunit of the slow delayed rectifier potassium channel. A normal corrected QT interval is less than 430 ms in males and 450 ms in females.

There are various causes of a prolonged QT interval, including congenital factors, drugs, and other medical conditions. Some drugs that can prolong the QT interval include amiodarone, tricyclic antidepressants, and selective serotonin reuptake inhibitors. Electrolyte imbalances, acute myocardial infarction, and subarachnoid hemorrhage can also cause a prolonged QT interval.

LQTS may be picked up on routine ECG or following family screening. The symptoms and events associated with LQTS can vary depending on the type of LQTS. Long QT1 is usually associated with exertional syncope, while Long QT2 is often associated with syncope following emotional stress or exercise. Long QT3 events often occur at night or at rest.

Management of LQTS involves avoiding drugs that prolong the QT interval and other precipitants if appropriate. Beta-blockers may be used, and in high-risk cases, implantable cardioverter defibrillators may be necessary. It is important to recognize and manage LQTS to prevent sudden cardiac death.

Based on the electrocardiogram (ECG) findings, the most likely diagnosis for this patient is an inferior myocardial infarction (MI), which occurs in the territory of the right coronary artery. This is indicated by ST-segment elevations in leads I, II, and aVF. Other ECG changes, such as complete heart block and bradycardia, may also be present due to the arterial supply the RCA gives to the atrioventricular and sinoatrial nodes. It is important to note that a new left bundle branch block (LBBB) may suggest acute coronary syndrome.

Acute pericarditis is unlikely as it presents with sharp retrosternal chest pain and a pericardial friction rub on auscultation, with different ECG findings such as widespread concave ST-segment elevations and PR segment depression.

An anterolateral MI would show ST-segment elevations in the anterolateral leads, while a posterior MI would show ST-segment depressions in the anterior leads with tall R waves.

In a pulmonary embolism (PE), ECG changes may include a large S wave in lead I, a large Q wave in lead III, and an inverted T wave in lead III – S1Q3T3, but this is only seen in a minority of patients. Most patients with a PE would have a normal ECG or sinus tachycardia, with signs of right-heart strain sometimes present. The clinical presentation of a PE would also differ from that of an MI, with symptoms such as tachypnea, tachycardia, lung crackles, fever, pleuritic chest pain, dyspnea, and hemoptysis.

Wolff-Parkinson-White (WPW) syndrome is a condition where there is an extra electrical pathway in the heart, making the patient more susceptible to developing supraventricular tachycardia (SVT). The presence of delta waves, which are a slurred upstroke in the QRS complex, and a shortened PR interval are characteristic of WPW syndrome. Atrial fibrillation (AF), on the other hand, is an irregularly irregular pulse that is diagnosed by the absence of P waves and irregular QRS complexes on an ECG. Delta waves are not typically seen in AF unless the patient also has WPW syndrome. Sinus arrhythmia, which is an irregular rhythm, does not show delta waves on an ECG. Acute myocardial infarction (MI) is not associated with delta waves, but rather with ST elevation or depression and T wave inversion. Supraventricular tachycardia (SVT) is a regular narrow complex tachycardia that may or may not have delta waves, depending on whether the patient has underlying WPW syndrome.

Torsades de pointes can be treated with IV magnesium sulfate.

Torsades de Pointes: A Life-Threatening Condition

Torsades de pointes is a type of ventricular tachycardia that is associated with a prolonged QT interval. This condition can lead to ventricular fibrillation, which can cause sudden death. There are several causes of a prolonged QT interval, including congenital conditions such as Jervell-Lange-Nielsen syndrome and Romano-Ward syndrome, as well as certain medications like antiarrhythmics, tricyclic antidepressants, and antipsychotics. Other causes include electrolyte imbalances, myocarditis, hypothermia, and subarachnoid hemorrhage.

The management of torsades de pointes involves the administration of intravenous magnesium sulfate. This can help to stabilize the heart rhythm and prevent further complications.

For the treatment of hypertension in diabetic patients, the first-line medication should be ACE inhibitors such as ramipril. However, this may not be suitable for individuals of Afro-Caribbean descent or women who may become pregnant. In case of a cough developing with ACE inhibitors, an angiotensin-II receptor antagonist like losartan should be prescribed. If the patient is not diabetic, calcium channel blockers like amlodipine or diuretics such as indapamide would be the preferred initial treatment. Beta blockers like propranolol are not typically the first choice for hypertension treatment, but may be considered for young patients who cannot tolerate ACE inhibitors or women attempting to conceive.

NICE released updated guidelines in 2019 for the management of hypertension, building on previous guidelines from 2011. These guidelines aimed to classify hypertension into stages and recommend the use of ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM) to accurately diagnose hypertension. This is important because some patients experience white coat hypertension, where their blood pressure rises in a clinical setting, leading to potential overdiagnosis of hypertension. ABPM and HBPM allow for a more accurate assessment of a patient’s overall blood pressure and can prevent overdiagnosis.

NICE recommends measuring blood pressure in both arms when considering a diagnosis of hypertension and repeating measurements if there is a difference of more than 20 mmHg between arms. If the blood pressure is >= 140/90 mmHg, NICE suggests offering ABPM or HBPM to confirm the diagnosis. If the blood pressure is >= 180/120 mmHg, referral for specialist assessment is recommended if there are signs of retinal haemorrhage or papilloedema or life-threatening symptoms. If target organ damage is identified, antihypertensive drug treatment may be started immediately.

ABPM involves taking at least 2 measurements per hour during the person’s usual waking hours and using the average value of at least 14 measurements. If ABPM is not tolerated, HBPM should be offered. HBPM involves taking two consecutive measurements at least 1 minute apart, twice daily for at least 4 days, and using the average value of all remaining measurements.

Interpreting the results of ABPM/HBPM is important for determining treatment. If the average blood pressure is >= 135/85 mmHg (stage 1 hypertension), treatment may be considered for patients under 80 years of age with target organ damage, established cardiovascular disease, renal disease, diabetes, or a 10-year cardiovascular risk equivalent to 10% or greater. In 2019, NICE also recommended considering antihypertensive drug treatment for adults under 60 with stage 1 hypertension and an estimated 10-year risk below 10%. If the average blood pressure is >= 150/95 mmHg (stage 2 hypertension), drug treatment should be offered regardless of age.

The National Institute for Health and Care Excellence recommends using a β blocker or calcium channel blocker as the first-line treatment for angina, along with a statin. If a patient is intolerant to β blockers or not responding to a CCB alone, a long-acting nitrate can be added. An ACE inhibitor is not indicated for angina treatment. Beta blockers and CCBs can be used together if one alone does not control symptoms, but caution is needed to avoid conduction problems. Long-acting nitrates should only be used in isolation if CCB or β blocker use is contraindicated. Aspirin is recommended for secondary prevention, and short-acting nitrates can be used for symptom relief. The 4S study showed that statins significantly reduce the risk of MI in patients with angina and high cholesterol levels.

Treatment Options for Deep Vein Thrombosis in Pregnancy

Start subcutaneous low molecular weight heparin (LMWH) throughout pregnancy and change to warfarin in the postpartum period: LMWH is recommended for the treatment of DVT during pregnancy. Treatment should be continued for at least three months and until six weeks postpartum. Warfarin can be used after day five of the postpartum period. Both LMWH and warfarin are safe to use while breastfeeding.

Elastic band compression of the affected leg, bedrest, and foot elevation: These measures have no benefit in treating DVT and may even increase the risk of developing a pulmonary embolism (PE) or another DVT.

Commence intravenous (IV) heparin: IV heparin can be used for the treatment of a shocked patient with PE if thrombolysis is not possible. It should not be used for DVT alone.

Oral anticoagulation with warfarin daily throughout pregnancy and the postpartum period: Warfarin is not recommended during pregnancy as it can cross the placenta and increase the risk of congenital malformations and bleeding.

Aspirin 300 mg daily throughout pregnancy and the postpartum period: Aspirin is not effective in treating DVT or PE as it is an antiplatelet drug, not an anticoagulant.

Treatment Options for Deep Vein Thrombosis in Pregnancy

Treatment Options for Aortic Stenosis

Aortic stenosis (AS) is a serious condition that requires prompt treatment. The gold standard treatment for symptomatic AS is surgical aortic valve replacement, which involves open-heart surgery and the use of mechanical or biological valves. However, for patients who are deemed too high risk for open-heart surgery, aortic balloon valvuloplasty or transcatheter aortic valve implantation (TAVI) may be considered as less invasive options.

Annual echocardiography monitoring is necessary to ensure the effectiveness of the treatment. It is important to note that oral nitrates are contraindicated in patients with AS as they can cause profound hypotension. Direct oral anticoagulants are also not licensed or indicated for the treatment of valvular heart disease. Overall, the choice of treatment depends on the patient’s individual risk factors and overall health status.

Hyperkalaemia is caused by ACE inhibitor.

Angiotensin-converting enzyme (ACE) inhibitors are commonly used as the first-line treatment for hypertension and heart failure in younger patients. However, they may not be as effective in treating hypertensive Afro-Caribbean patients. These inhibitors are also used to treat diabetic nephropathy and for secondary prevention of ischaemic heart disease. The mechanism of action of ACE inhibitors is to inhibit the conversion of angiotensin I to angiotensin II. They are metabolized in the liver through phase 1 metabolism.

ACE inhibitors may cause side effects such as cough, which occurs in around 15% of patients and may occur up to a year after starting treatment. This is thought to be due to increased bradykinin levels. Angioedema may also occur up to a year after starting treatment. Hyperkalaemia and first-dose hypotension are other potential side effects, especially in patients taking diuretics. ACE inhibitors should be avoided during pregnancy and breastfeeding, and caution should be exercised in patients with renovascular disease, aortic stenosis, or hereditary or idiopathic angioedema.

Patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day) are at an increased risk of hypotension when taking ACE inhibitors. Before initiating treatment, urea and electrolytes should be checked, and after increasing the dose, a rise in creatinine and potassium may be expected. Acceptable changes include an increase in serum creatinine up to 30% from baseline and an increase in potassium up to 5.5 mmol/l. Patients with undiagnosed bilateral renal artery stenosis may experience significant renal impairment. The current NICE guidelines provide a flow chart for the management of hypertension.