CC/4 Complaints of burning and pressing pains in the chest lasting abo

CC/4 Complaints of burning and pressing pains in the chest lasting about an hour, pain in the left shoulder and left arm, shortness of breath, fear, headache, sudden weakness and sweating. Medical history: high blood pressure for about 7 years, registered with a clinic, undergoes regular check-ups, takes antihypertensive drugs. Yesterday, he felt general discomfort and a burning sensation in his chest, but after a while it went away. Today, the burning pain behind the breastbone reappeared, he took nitroglycerin under the tongue twice, but the pain intensified, he felt short of breath and broke out in a cold sweat. His relatives called an ambulance. Anamnesis: 68 years old. For 5-6 years, he has had osteoarthritis of the large and small joints, with pain in the joints of the feet being particularly troublesome, limiting his ability to walk. In recent years, he has gained a lot of weight, which he attributes to walking less. He has been a long-term smoker and is a moderate drinker. He works as a bus driver. Family history: his brother had a myocardial infarction at the age of 53. Allergic history: no significant history. Objectively: Moderate condition due to severe pain syndrome. Consciousness is clear. BMI is 30 kg/m2. Skin is pale, with cold, clammy sweat. Peripheral lymph nodes are not palpable. Auscultatory: vesicular breathing, no rales. RR 19 per minute. Boundaries of relative cardiac dullness within age norms. Heart sounds sharply muffled, tachycardia with HR 90 beats per minute. BP 100/60 mm Hg on both arms. Tongue is clean. Abdomen is soft on palpation. Liver is at the edge of the costal arch. Percussion symptom is negative on both sides. Urination is free and painless. Laboratory and diagnostic tests: Complete blood count: haemoglobin 142 g/l, haematocrit - 40%, erythrocytes - 5.15*10¹²/1, leukocytes 6.25*10/1, thrombocytes-289*109/1, ESR-15 mm/h. Urinalysis: pH 5.0, relative density 1.020, colour yellow, white blood cells 1-2 per field of view, epithelium 0-1 per field of view, protein - negative, glucose negative, ketones - negative. Biohemical test: Glucose 4.9 mmol/l, Low-density lipoproteins (LDL) 4.16 mmol/l, high-density lipoproteins (HDL) 0.85 mmol/l, creatinine 69.2 µmol/l, uric acid 525 µmol/l, total bilirubin - 7.15 µmol/l, Total cholesterol 6.32 mmol/l, Triglycerides 3.45 mmol/l, Fibrinogen 4.65 g/l, Troponin I-0.28 ng/ml. FCG: AVR aVL aVF Assignment for student: 1. Establish and justify the complete clinical diagnosis according to the latest international classification, specifying the disease activity, complications of the underlying disease (if present), and comorbidities (if present). Do not use abbreviations or acronyms. 2. Interpret the data of all presented laboratory analyses and instrumental examination methods. What laboratory and instrumental methods should be added, and what changes are characteristic of this disease? 3. Determine the management and treatment strategy for the patient, including non-pharmacological and pharmacological interventions. Specify the therapeutic classes and names of drugs for etiological, pathogenetic, symptomatic, and/or replacement therapy, and provide a comprehensive plan for annual follow-up and routine monitoring.

Reading File

Quick answer

1. Working clinical diagnosis

Acute non-ST-segment elevation myocardial infarction, type 1, due to suspected acute atherothrombotic coronary artery disease, with ongoing ischemic chest pain. Killip class I, without clinical heart failure or cardiogenic shock.

Major cardiovascular risk factors and comorbidities:

Essential arterial hypertension, treated, duration about seven years. Current blood pressure is low-normal in the acute setting.
Mixed atherogenic dyslipidemia: increased total cholesterol, low-density lipoprotein cholesterol and triglycerides, with reduced high-density lipoprotein cholesterol.
Obesity, class I, body mass index 30 kilograms per square meter.
Long-term tobacco dependence.
Family history of premature coronary artery disease: brother sustained myocardial infarction at age 53 years.
Hyperuricemia without documented gout.
Osteoarthritis of large and small joints, with reduced mobility.
Sedentary occupation and limited exercise capacity.

Justification

The diagnosis is strongly supported by:

Typical prolonged ischemic pain: severe retrosternal burning and pressing pain lasting about one hour, radiating to the left shoulder and arm.
Autonomic symptoms: cold sweat, pallor, intense fear, weakness, dyspnea.
Failure of two doses of sublingual nitroglycerin to relieve pain.
Troponin I of 0.28 nanograms per milliliter, which is elevated for most laboratory assays and indicates myocardial injury.
Numerous atherosclerotic risk factors: age, male sex, hypertension, smoking, obesity, dyslipidemia, poor mobility, and premature family history.

The supplied electrocardiographic material is incomplete: only limb-lead labels are shown, without interpretable tracings. Therefore, ST-segment elevation cannot be confirmed or excluded from the material provided. A full immediate twelve-lead electrocardiogram and serial recordings are essential. If persistent ST-segment elevation or a new left bundle branch block equivalent is found, the diagnosis and reperfusion pathway change to acute ST-segment elevation myocardial infarction.

2. Interpretation of findings and additional investigations

Clinical findings

Finding	Interpretation
Pale skin, cold clammy sweat, severe ongoing pain	Typical sympathetic response to acute myocardial ischemia
Respiratory rate 19 per minute, clear lungs	Mild dyspnea without signs of pulmonary edema
Heart rate 90 beats per minute	Relative tachycardia in an acute coronary syndrome
Blood pressure 100/60 millimeters of mercury	Borderline blood pressure. Nitrates and beta blockers must be used cautiously
Muffled heart sounds	Nonspecific; requires echocardiographic assessment
No crackles, no peripheral edema	No clinical evidence of acute left ventricular failure, consistent with Killip class I
Body mass index 30 kilograms per square meter	Class I obesity

Complete blood count

Hemoglobin 142 grams per liter, hematocrit 40 percent, erythrocytes 5.15 × 10¹² per liter: no anemia. This is important because anemia can worsen myocardial ischemia.
Leukocytes 6.25 × 10⁹ per liter: no leukocytosis.
Platelets 289 × 10⁹ per liter: normal baseline platelet count, allowing antiplatelet and anticoagulant treatment unless other contraindications appear.
Erythrocyte sedimentation rate 15 millimeters per hour: nonspecific and not diagnostically important in acute coronary syndrome.

Urinalysis

Essentially normal:

No proteinuria, glucosuria, ketonuria, or significant leukocyturia.
Specific gravity 1.020 and pH 5.0 are compatible with adequately concentrated acidic urine.
There is no evidence of urinary infection, overt renal disease, or diabetes-related glucosuria.

Biochemical testing

Test	Result	Interpretation
Glucose	4.9 millimoles per liter	Normal at presentation
Creatinine	69.2 micromoles per liter	Renal function appears preserved. Calculate estimated glomerular filtration rate before contrast angiography and anticoagulant dosing
Troponin I	0.28 nanograms per milliliter	Myocardial injury. Serial testing is required to document a rise or fall and confirm acute myocardial infarction
Total cholesterol	6.32 millimoles per liter	Elevated
Low-density lipoprotein cholesterol	4.16 millimoles per liter	Markedly elevated for a patient with established acute coronary syndrome
High-density lipoprotein cholesterol	0.85 millimoles per liter	Reduced
Triglycerides	3.45 millimoles per liter	Elevated
Fibrinogen	4.65 grams per liter	Elevated acute-phase and prothrombotic marker
Uric acid	525 micromoles per liter	Hyperuricemia, likely contributed to by obesity, diet, alcohol, and reduced activity
Bilirubin	7.15 micromoles per liter	Within or near the lower end of the usual reference range, not clinically significant here

The lipid profile is highly atherogenic and requires intensive lipid-lowering treatment after acute stabilization.

Investigations required immediately

Twelve-lead electrocardiogram immediately, interpreted within 10 minutes of first medical contact.
Repeated twelve-lead electrocardiograms during recurrent pain and after symptom changes.
Serial high-sensitivity cardiac troponin testing, preferably at presentation and one to three hours later, using the same assay.
Continuous cardiac rhythm and ST-segment monitoring to detect ventricular arrhythmias, bradyarrhythmias, ischemic changes, or atrioventricular block.
Transthoracic echocardiography to assess:
- Left ventricular ejection fraction.
- Regional wall-motion abnormality.
- Papillary muscle dysfunction and mitral regurgitation.
- Pericardial effusion.
- Alternative causes of chest pain, if relevant.
Urgent invasive coronary angiography with intent to perform percutaneous coronary intervention because this patient has ongoing/recurrent ischemia and elevated troponin.
Coagulation studies: prothrombin time, international normalized ratio, activated partial thromboplastin time.
Repeat renal function, electrolytes, magnesium, potassium, liver enzymes, and blood glucose.
Glycated hemoglobin to identify unrecognized diabetes mellitus.
Chest radiograph if dyspnea worsens or heart failure, pneumonia, aortic disease, or another thoracic diagnosis is suspected.
If diagnosis remains uncertain, consider D-dimer testing and computed tomographic angiography only when pulmonary embolism or acute aortic syndrome is clinically plausible. These must not delay coronary reperfusion in a likely infarction.

Expected electrocardiographic and imaging changes

In non-ST-segment elevation myocardial infarction, common electrocardiographic patterns include:

ST-segment depression.
T-wave inversion.
Transient ST-segment elevation that resolves.
A normal or nonspecific electrocardiogram early in the course.

Echocardiography may show regional hypokinesia, akinesia, or dyskinesia in the territory supplied by the affected coronary artery. A normal echocardiogram does not exclude non-ST-segment elevation myocardial infarction.

3. Management and treatment strategy

This patient requires immediate admission to a coronary care unit. Persistent chest pain, positive troponin, and high clinical risk require urgent cardiology evaluation and coronary angiography.

Immediate non-pharmacological management

Strict rest with continuous cardiac monitoring.
Two large-bore intravenous lines.
Frequent measurement of blood pressure, heart rate, oxygen saturation, urine output, and pain.
Defibrillator access and readiness for advanced cardiac life support.
Oxygen only if oxygen saturation is below 90 percent, respiratory distress is present, or there is pulmonary edema. Routine oxygen in a normally oxygenated patient is not recommended.
Keep the patient fasting pending urgent coronary angiography.
Do not allow smoking.
Avoid nonsteroidal anti-inflammatory drugs, except low-dose aspirin prescribed for the acute coronary syndrome, because these drugs increase cardiovascular risk and can worsen renal function and blood pressure.

Acute pharmacological treatment

Antiplatelet treatment

Aspirin
- Loading dose: 150 to 300 milligrams orally chewed, or 75 to 250 milligrams intravenously if oral treatment is impossible.
- Maintenance: 75 to 100 milligrams once daily lifelong, unless contraindicated.
A P2Y12 receptor inhibitor
- If an invasive strategy with coronary intervention is expected, an appropriate option is ticagrelor, 180 milligrams loading dose followed by 90 milligrams twice daily.
- Prasugrel may be selected after coronary anatomy is known and if percutaneous coronary intervention is planned, provided there is no previous stroke or transient ischemic attack and bleeding risk is acceptable.
- Clopidogrel is an alternative when ticagrelor or prasugrel is contraindicated, unavailable, poorly tolerated, or bleeding risk is high.

Dual antiplatelet therapy is generally continued for 12 months after acute coronary syndrome, then reassessed according to ischemic and bleeding risk.

Anticoagulant treatment

Give anticoagulation unless contraindicated:

Unfractionated heparin, especially if urgent coronary angiography and percutaneous coronary intervention are planned.
Alternative options in selected patients include enoxaparin or fondaparinux. If fondaparinux is used and percutaneous coronary intervention occurs, additional unfractionated heparin is required during the procedure.

Dose selection depends on weight, kidney function, age, bleeding risk, and the invasive strategy.

Anti-ischemic and analgesic treatment

Sublingual nitroglycerin can be considered only if systolic blood pressure remains safely above 90 to 100 millimeters of mercury and there is no right ventricular infarction, recent phosphodiesterase type 5 inhibitor use, or severe aortic stenosis.
This patient has blood pressure of 100/60 millimeters of mercury and worsening pain after two doses. Do not continue repeated nitrate doses without close hemodynamic supervision.
If severe pain continues despite anti-ischemic therapy, use carefully titrated intravenous morphine with monitoring for hypotension and respiratory depression.
A beta blocker such as metoprolol is appropriate after stabilization if there is no hypotension, acute heart failure, bradycardia, high-grade atrioventricular block, bronchospasm, or shock risk. It should not be started aggressively while blood pressure is borderline.

Lipid-lowering treatment

Start high-intensity statin therapy immediately:

Atorvastatin 80 milligrams once daily, or
Rosuvastatin 20 to 40 milligrams once daily.

The target is at least a 50 percent decrease in low-density lipoprotein cholesterol and an absolute low-density lipoprotein cholesterol level below 1.4 millimoles per liter. If the target is not reached after four to six weeks, add ezetimibe. If still above target, consider a proprotein convertase subtilisin/kexin type 9 inhibitor.

Renin-angiotensin-aldosterone system blockade

After blood pressure stabilizes:

Start an angiotensin-converting enzyme inhibitor such as ramipril or perindopril, especially because of hypertension and high cardiovascular risk.
Use an angiotensin receptor blocker if an angiotensin-converting enzyme inhibitor is not tolerated.
Add a mineralocorticoid receptor antagonist, such as eplerenone, if left ventricular ejection fraction is 40 percent or less and there is heart failure or diabetes, provided potassium and renal function allow it.

Revascularization

The preferred strategy is urgent invasive coronary angiography followed, when appropriate, by percutaneous coronary intervention with coronary stenting.

Immediate angiography is particularly indicated if pain persists or recurs despite treatment, there are dynamic electrocardiographic changes, hemodynamic instability, malignant arrhythmia, or acute heart failure. If none of these are present after stabilization, a high-risk non-ST-segment elevation myocardial infarction should still undergo early angiography, usually within 24 hours.

Fibrinolytic therapy is not indicated for non-ST-segment elevation myocardial infarction.

Secondary prevention and annual follow-up

Lifestyle and rehabilitation

Complete smoking cessation. Offer behavioral treatment plus pharmacotherapy such as nicotine replacement therapy, varenicline, or bupropion where suitable.
Enroll in supervised cardiac rehabilitation after stabilization.
Mediterranean-style eating pattern: vegetables, fruit, legumes, whole grains, fish, nuts, unsaturated fats; sharply reduce processed foods, trans fats, refined sugar, and excess salt.
Gradual weight reduction toward a body mass index below 25 kilograms per square meter.
Alcohol: preferably avoid it during early recovery; thereafter, do not recommend alcohol for cardiovascular protection.
Exercise prescription after rehabilitation assessment. His osteoarthritis may require low-impact activity, such as stationary cycling, water exercise, or supervised walking.
Avoid self-treatment of joint pain with nonsteroidal anti-inflammatory drugs. Discuss safer analgesic options with the physician.

Monitoring schedule

Before discharge

Repeat electrocardiogram.
Echocardiography.
Renal function, electrolytes, complete blood count, lipid profile, glucose.
Review of coronary angiography result, stent status, and prescribed antithrombotic plan.
Counseling regarding medication adherence, bleeding warning signs, recurrent angina, and emergency response.

At 1 to 2 weeks

Assess recurrent chest pain, dyspnea, blood pressure, heart rate, medication adherence, bleeding, and adverse drug effects.
Check creatinine and potassium after initiation or dose change of angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, or mineralocorticoid receptor antagonist.

At 4 to 6 weeks

Fasting lipid profile.
Liver enzymes if clinically indicated after statin therapy.
Review low-density lipoprotein cholesterol response and intensify lipid therapy if target is not met.
Assess smoking cessation and participation in cardiac rehabilitation.

At 3 months

Blood pressure, body weight, symptoms, functional capacity, drug adherence, and adverse effects.
Repeat renal function and electrolytes.
Glycated hemoglobin if elevated initially or if diabetes risk remains high.

Every 6 to 12 months

Cardiovascular review, blood pressure, pulse, body mass index, smoking status, exercise, diet, and medication adherence.
Lipid profile until goal is achieved, then at least annually.
Renal function, potassium, complete blood count when clinically indicated, particularly during antithrombotic treatment.
Evaluation for heart failure, recurrent angina, arrhythmia, stroke symptoms, peripheral arterial disease, and bleeding.
Annual influenza vaccination and age-appropriate pneumococcal vaccination.

Urgent reassessment is required for recurrent chest pressure, breathlessness at rest, syncope, palpitations, black stools, vomiting blood, or new neurologic symptoms.

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