Atherosclerotic CVD and Myocardial infarction- 2 - Free MCQ Practice Test

• Dressler’s syndrome is also known as post-myocardial infarction syndrome and the term is sometimes used to also refer to post-pericardiotomy pericarditis which is a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium.
• It consists of a triad of features, fever, pleuritic pain and pericardial friction rub/pericardial effusion.
• It is believed to result from an autoimmune inflammatory reaction to myocardial neo-antigens formed as a result of the MI.
• A similar pericarditis can be associated with any pericardiotomy or trauma to the pericardium or heart surgery.

RVMI leads to decreased pulmonary flow and hypotension on presentation. RVF explains then kussmaul sign.

LDH 2 is the primary form found in serum, while LDH 1 is mainly located in the heart and red blood cells. Therefore, under normal circumstances, LDH 2 levels are greater than LDH 1. In the event of a myocardial infarction (MI), damaged myocytes lead to the release of LDH 1 into the bloodstream, causing the serum levels of LDH 1 to exceed those of LDH 2. This pattern, where LDH 1 is greater than LDH 2, is referred to as the Flipped pattern. However, currently, troponin levels are measured after an MI instead of the values for LDH 1 and LDH 2.
Role of LDH currently as tumour marker In:
1. Lymphoma
2. Ewing Sarcoma
3. Hepatitis
4. Haemolytic Anaemia
Isoenzymes

• Isoenzymes are multiple enzyme, isomers of enzyme
• There are five isoenzymes of LDH
• LDH-1 found In heart and in RBC as well as in brain
• LDH-2 found In the reticuloendothelial system 
• LDH 3 found In the lungs
• LDH-4 found In the kidneys, placenta and pancreas
• LDH 5 found In the liver and striated muscle

The lipid profile report for the patient indicates raised levels of LDL and triglycerides. This suggests a diagnosis of Type IIB hyperlipoproteinemia. The patient has already experienced atherosclerotic cardiovascular disease. Therefore, high-dose statins should be initiated to mitigate the future development of atherosclerotic plaques in the coronary circulation.

• High-intensity statins recommended include:
  • Atorvastatin 40-80 mg
  • Rosuvastatin 20-40 mg
• Fenofibrates are indicated if triglyceride levels exceed 500 mg%.

Guidelines for use of high dose statins
1. ASCVD (Ml/ unstable angina/ Chronic stable angina/ Stroke/ TIA episodes/ PVD)
2. Asymptomatic with age > 21years and LDL > 190mg/dl
3. LDL > 70 with DM
4. LDL >70 with age > 40 years
5. 10 year CV risk by Framingham score of > 7.5%

The patient has a history of chronic stable angina and has now developed unstable angina due to the episodes becoming more severe, frequent, and occurring even at rest.

• Anti-thrombotic treatment involving heparin, abciximab, and an intravenous beta blocker is advised.
• The TIMI score will be calculated to determine if a revascularisation procedure is necessary.
• Thrombolysis is not suitable for unstable angina.

The RCA provides blood flow to the majority of the inferior myocardium. In approximately 60% of patients, the proximal section supplies the SAN, while in about 90% of patients, the distal section supplies the AV node. Therefore, an obstruction in the RCA can result in bradycardia.

• The injured RV can irritate the diaphragm.
• This irritation may result in hiccups.

The clinical presentation involves variant angina. The patient will be treated with long-acting nitrates and CCB to avert the onset of spasms in the epicardial coronary artery.

Following this, a coronary angiography will determine the appropriate type of revascularisation procedure.

• Options B and D are applicable for chronic stable angina.
• Option A will provide no diagnostic assistance.

The patient presents with all significant risk factors for the development of an abdominal aortic aneurysm. If the size of the AAA surpasses 5.5 cm, surgical intervention is advised. Additional reasons for surgery include:

• Rapid expansion
• Onset of symptoms

Endovascular stent grafts for infra-renal AAA are proving effective in certain patients.
Risk of rupture of abdominal aorta aneurysm

Plasma ET-1 levels increase following an acute myocardial infarction, attributed to coronary vasoconstriction, which leads to myocardial ischaemia and ventricular dysfunction.
Endothelin (ET)-1 acts as a strong coronary vasoconstrictor.

The VLDL cholesterol is calculated by taking the plasma triglyceride concentration and dividing it by 5. This represents the relationship between TG and cholesterol within VLDL particles.

The Friedewald formula is utilised to determine the level of LDL-Cholesterol. The equation for LDL is:

• LDL = Total cholesterol - TG/5 - HDL.

It is essential to collect samples for lipid and lipoprotein levels after a fasting period of 12 hours. The Friedewald formula will provide an accurate LDL calculation if the triglyceride level is below 200 mg/dl. By standard practice, this formula is not applied if triglyceride levels exceed 200 mg/dl. The 10-year mortality risk related to atherosclerotic cardiovascular disease is assessed using the Framingham risk calculator.

• Hyperalphalipoproteinemia results in increased concentrations of Apo-A I and Apo-A II, leading to higher HDL levels.
• Individuals with Hyperalpha-Lipoproteinemia typically do not exhibit any unusual clinical symptoms.
• This condition should not be regarded as a disease but rather as a fortunate circumstance that can enhance longevity due to its association with a lower incidence of CHD.

• This condition manifests in infancy with symptoms such as diarrhoea and fat malabsorption.
• Neurological symptoms may arise, including loss of deep tendon reflexes, reduced vibration sensation, and impaired proprioception.
• A spastic gait may develop, accompanied by pigmentary retinopathy, which leads to diminished night and colour vision.

• Patients typically present with multiple tendon xanthomas despite having normal cholesterol levels.

The image depicts a child exhibiting erythema on the cheeks, along with signs of stomatitis. The angiography results indicate several aneurysms along the left main coronary artery. Therefore, the diagnosis is Kawasaki disease.

• Choice A is incorrect as aspirin helps prevent the onset of myocardial infarction in individuals with Kawasaki disease.
• Choice B is also incorrect because patients present with bulbar congestion but do not show any discharge.
• Choice D is wrong as well, as patients typically develop unilateral cervical lymphadenopathy accompanied by fever during the early stages of the illness.

• The presence of milky plasma and abdominal discomfort in the child suggests increased triglyceride levels, potentially leading to acute pancreatitis.
• Milky plasma is observed in type I and type V hyperlipoproteinaemia.
• Xanthomas are identified in type I, IIa, III, and type V hyperlipoproteinaemia.
• The combination of milky plasma and xanthomas occurs in type I and type V hyperlipoproteinaemia.
• In both cases, chylomicrons are elevated; however, in type V, both chylomicrons and VLDL levels are increased.

• Right ventricular (RV) infarction is seldom seen in isolation, with about one-third to half of patients experiencing inferior-wall myocardial infarction (IWMI) showing some degree of RV involvement (Choice A).
• In clinical settings, RV infarction is often identified through electrocardiography. A significant ST-segment elevation of >1 mm in lead V4R is indicative and closely associated with other noninvasive indicators of RV dysfunction (Choice B).
• Patients suffering from acute IWMI face a significantly higher risk of mortality during hospitalisation if RV involvement is detected (Choice C).
• The clinical triad of hypotension, clear lung fields, and increased jugular venous pressure has traditionally been regarded as a marker for RV infarction in individuals with IWMI.
• Diltiazem may exacerbate the hypotension associated with right ventricular infarction.

The patient's heart rate is approximately 75 BPM. The current ECG displays ST elevation in lead I, aVL, and the precordial leads V₂-V₅, indicating an anterior wall myocardial infarction (MI).

• Heart rate is recorded as 45/min, which is incorrect.
• The patient should receive lidocaine, typically administered for post-MI ventricular tachycardia.
• The ECG suggests hyperkalemia.
• ST elevation and prominent tented T waves should be observed in all leads.
• The P wave may vanish.
• The QRS complex will be wide.

Regular rhythms can be quickly assessed by counting the number of large graph boxes between two R waves. This figure is then divided into 300 to determine BPM.

The prevalent form of dyslipidemia observed in diabetes mellitus is:

• hypertriglyceridemia
• decreased HDL levels

Primary percutaneous coronary intervention (PCI) is the recommended treatment for ST segment elevation myocardial infarction, aiming to ensure that the time from door to device is under 90 minutes.

• SPECT using thallium₂₀₁
• Technetium^99m with either exercise or pharmacologic stress
• PET Myocardial perfusion imaging

• Rubidium⁸²
• 13-N ammonia
• 18F-fluorodeoxyglucose (FDG), which evaluates myocardial glucose metabolism and serves as an indicator of viability

• Statins, specifically at a dosage of atorvastatin 80 mg, offer long-term mortality advantages.
• Aspirin, when taken daily, decreases the frequency of clinical events and enhances survival rates.
• Other oral antiplatelet medications, such as clopidogrel, abciximab, tirofiban, and eptifibatide, also contribute to improved survival.

• In cases of mitral stenosis, the left ventricular muscle function is typically normal, making digitalis of minimal value for patients in sinus rhythm.
• However, in individuals with atrial fibrillation, digitalis is employed to manage and reduce the ventricular rate.
• A rapid ventricular rate in mitral stenosis leads to a shortened diastolic phase, which diminishes left ventricular filling.
• This reduction in filling consequently raises left atrial pressure and decreases cardiac output.

• Niacin, fibrates, and prescription omega-3 fatty acids are approved for managing hypertriglyceridemia.
• Statins, or HMG-CoA reductase inhibitors, are a category of cholesterol-lowering medications that block the enzyme HMG-CoA reductase, which is crucial for cholesterol production.
• Ezetimibe works by preventing the absorption of cholesterol in the small intestine, thereby reducing the amount of cholesterol available to liver cells, prompting them to take up more from the bloodstream and consequently lowering circulating cholesterol levels.

• Cardiac markers play a crucial role in diagnosing and assessing the risk of patients experiencing chest pain and suspected acute coronary syndrome (ACS).
• The cardiac troponins, in particular, have become the cardiac markers of choice for patients with acute coronary syndrome which includes NSTEMI.
• Indeed, cardiac troponin is central to the definition of acute myocardial infarction (MI) in the consensus guidelines from the European Society of Cardiology (ESC) and the American College of Cardiology (ACC).
• However in chronic Stable angina the symptoms arise on exertion/emotion or post-prandially and have characteristic ST segment depression on exercise testing. Cardiac biomarkers arc normal as no cell death occurs in this case.

• Post-pericardiotomy syndrome following myocardial infarction is called Dressler syndrome and is an autoimmune process.
• It also seen as an unusual complication after percutaneous procedures such as coronary stent implantation, after implantation of epicardial pacemaker leads and transvenous pacemaker leads, and following blunt trauma,stab wounds.and heart puncture.
• It involves the pleura and pericardium and is also seen in patients who have undergone surgery that involves opening the pericardium.

• ACEIs attenuate the development of left ventricular hypertrophy, improve symptomatology and risk of death from CHF, and reduce morbidity and mortality rates in post-myocardial infarction patients
• Similar benefits in cardiovascular morbidity and mortality rates in patients with CHF have been observed with the use of ARBs.
• ACEIs provide better coronary protection than do calcium channel blockers, whereas calcium channel blockers provide more stroke protection than do either ACEIs or beta blockers.

Aspirin and clopidogrel have been shown to reduce mortality due to MI.

• Statins regress atherosclerosis and β blockers due to oxygen conserving action will prevent future episode of MI.
• Warfarin is not routinely used in post MI Patients.

• Alcohol in mild amounts has been shown to have beneficial effect on heart.
• Studies have shown chylamydia as incriminating factor for atherosclerosis and so does poor dental hygiene.

• The ECG shows patient in sinus Rhythm, normal QRS axis.
• Upsloping ST segment elevation is seen in V2-V5 and aVL.
• In extreme left premature ventricular beats can be noticed in Lead II and Lead III.
• Rhythm strip lead II shows ST depression (right at the bottom).
• Brugada syndrome has ST elevation in V1-V3 and can present with sudden collapse during physical exertion but the collapse occurs due to ventricular tachycardia. ECG strip however docs not show any tachyarrhythmia.
• Arrythmogenic right ventrcular dysplasia shows presence of epsilon waves.