INTERNAL MEDICINE CASE PRESENTATION

BY: AKSHAY MAURYA

Clinical Case

ISCHEMIC HEART DISEASE.

Attending Physician – DR. CAMPS

This is a case report of a patient with ischemic heart disease, NYHA II, that does not admit to
any past cardiovascular medical history but is currently on medication for heart failure.

ABSTRACT
This article seeks to discuss the management of a stable heart failure patient and review the
recent discoveries in the management of heart failure. It also mentions some of the etiologies,
risk factors, signs and symptoms of heart failure.

CASE REPORT
XYZ is a 55 years old male patient that lives in cross street Lipol, Georgetown. He owns a shop
and that is where he works. He came for a regular heart function clinic visit complaining of
shortness of breath, paroxysmal nocturnal dyspnea, chest pain, occasional palpitations and
intermittent productive cough that have been going on for two months.He has no dizziness and
he sometimes vomits. He has good appetite and carries out his normal daily routine without
difficult.
He has was diagnosed with tuberculosis in 2016 due to persistent coughing. He was given
treatment for the same but he did not get better. It was then discovered that he had
cardiomegaly. He was diagnosed with heart failure due to cardiomegaly in august this year and
started on medication but he declined from taking it due to vomiting. When his symptoms
exacerbated in September he came to accident and emergency and was managed as an acute
heart failure patient. He was discharged with T. Hydralazine 25mg PO TID, T. Metoprolol 25mg
PO BID, T. Atorvastatin 40mg PO BID, T. Lasix 40mg PO BD, Losartan, Aspirin, Isordil. HTCZ
and referred to the heart function clinic. He has since been taking these medications.
His mother is diabetic and hypertensive while his father is diabetic. There is no one in the family
that has had heart failure. He had a stab wound to his abdomen two years ago that required
surgery. He used to take alcohol for one year but no longer does and he does not smoke.
Physical examination
General appearance: Patient appears well groomed, tired and sleepy.
Vitals: HR-80bpm, BP-110/80mmHg, SpO2-99%, RR-19bpm, weight-250Ibs, Height-60inches.
Head: normocephalic, eyes, ears, throat are normal
Neck: no distended neck veins
Resp: BAE, Lungs are clear
CVS: S2 S3, no murmur, has a JVP of 4cm
Abd: Has a midline incision, normal bowel sounds, no ascites, no tenderness, hepatojugular
reflex is negative
Ext: Has pretibial edema to both lower extremities +1, no clubbing and no cyanosis.
CNS: alert and conscious

Investigations
His initial investigations were done in august and were remarkable for high triglycerides, VLDL,
BUN and creatinine. His HbA1C was 6.40%.
His echo revealed a mildly dilated left ventricle with mild concentric left ventricular hypertrophy
and severe global systolic dysfunction. The inferior septum wall and the mid-apical inferolateral
segments were akinetic. There was severe hypokinesis of the remaining ventricle. His estimated
LVEF was 15-25%. He has a normal right ventricular chamber size with mild global systolic
dysfunction. He had moderate tricuspid regurgitation into a mildly dilated right atrium and his
pulmonary artery systolic pressure was mildly elevated. He also had moderate mitral
regurgitation into a moderately dilated left ventricle with IAS bowing towards the RA. He had
sinus rhythm.
His ECG showed sinus tachycardia, bi-atrial enlargement, ST & T wave abnormality most likely
due to inferolateral ischemia.
His chest x-ray revealed cardiomegaly with mild congestion.
His most recent blood workup results are remarkable for low HDL and high BUN and uric acid.
Primary impression
55 years old male with stable Left ventricular heart failure due to ischemic heart disease. NYHA
II
Final diagnosis
55 years old male with stable Left ventricular heart failure due to ischemic heart disease. NYHA
II
Management
He is being managed with T. Metoprolol 50mg BD, T. Losartan 25mg BD, T. Furosemide 40mg
BD, T. Spironolactone 25mg OD, Hydralazine 25mg TID, T. Isordil 10mg TID, T. Aspirin 81mg
OD, T. Atorvastatin 40mg OD

DISCUSSION
‘Heart failure develops when the heart, via an abnormality of cardiac function (detectable or
not), fails to pump blood at a rate commensurate with the requirements of the metabolizing
tissues or is able to do so only with an elevated diastolic filling pressure.’(1) Heart failure can
occur due to decreased cardiac output or increased cardiac demand. A low cardiac output
results from a systolic dysfunction or a diastolic dysfunction. A systolic dysfunction occurs when
there is ineffective ventricular contraction while a diastolic dysfunction occurs when there is
ineffective ventricular filling. (2) In this case, the patient has systolic dysfunction. He has a mild
left ventricular dilation and mild left ventricular hypertrophy according to his echo report. This
isas a result of an injury and ischemia in the myocardium leading to inflammation, infiltration and
fibrosis. This caused mild dilation and stiffening of the myocardium and as a result he has
ineffective ventricular contraction. These mechanisms increase the cardiac workload and cause
myocardial stress, volume overload or pressure overload. The body responds by activating the
sympathetic nervous system and renin angiotensin aldosterone system. Sodium and water are
retained increasing the preload and afterload and the cycle of increased cardiac demand and
decompensation is perpetuated. (2)Compensated heart failure means the patient is stable with
lack of fluid retention in the lungs, whereas decompensated heart failure means the patient is
unstable with lots of fluid retention in the lungs, deterioration of heart function and his heart is
unable to maintain blood circulation. (3, 2)Both the compensated and decompensated patient
require treatment for the symptoms they may be experiencing. In this case, our patient is stable
and his lungs are clear, therefore, he has stablecompensated heart failure.
There are various etiologies of heart failure. Heart failure can be due to an underlying cause, a
fundamental cause, a precipitating cause or a genetic cardiomyopathy.Depending on the
etiology, patients will initially present with different signs and symptoms but as the condition
progresses and a diagnosis of heart failure is made, patients have common signs and
symptoms including shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, coughing,
chest pain, palpitations edema etc. Some causes of heart failure include hypertension, valvular
diseases, ischemic heart disease, diabetes mellitus, anemia, pulmonary hypertension and
several others. (1) There are certain risk factors for heart failure such as age (>40 for male, > 55
for females), gender (male to female ratio of 8:1), smoking, high alcohol intake, family history of
heart disease, high LDL, stress, sedentary lifestyle, diabetes etc. (4) This patient’s risk factors
are age (>40), gender, previous heavy alcohol intake and hyperlipidemia. His heart failure is a
result of ischemic heart disease due to hyperlipidemia. Currently he is experiencing shortness of
breath, Paroxysmal nocturnal dyspnea, chest pain, occasional palpitations and intermittent
productive cough. The New York heart association(NYHA) functional classification of heart
failure has four stages. Class I patients are able to perform ordinary physical activity and are
asymptomatic.Class II patients are comfortable at rest and performing ordinary physical activity
results in symptoms. Class III patients have marked limitation ofordinary activity and performing
less than ordinaryphysical activity results in symptoms. Class IV patients are unable to carry
out anyphysical activity without discomfort and symptoms may be present at rest. Left
ventricular dysfunction is measured using the ejection fraction. Grade I (EF >60%) (Normal),
Grade II (EF = 40-59%), Grade III (EF = 21-39%) and Grade IV (EF ≤20%). This patient has
NYHA class II with an estimated LVEF of 15-25%.
The pharmacological therapy for heart failure focuses on controlling the risk factors, alleviating
symptoms and reducing mortality. Angiotensin converting enzyme inhibitors, beta-blockers and
aldosterone antagonists have shown to reduce mortality.However, currently no proven
pharmacologic therapies have shown to reduce mortality in heart failure with reduced ejection
fraction. (2) Lifestyle measures such as diet, exercise, diabetes control, smoking cessation,
decreased alcohol consumption,patient education, sodium and fluid restriction have to be
undertaken. The patients also have to report to a multidisciplinary heart failure clinic for follow
up to monitor their progress (whether better or worse). According to a study conducted by
Cooper et.al assessment of patient-reported social support and perceived barriers may facilitate
individualized approaches to implement and sustain exercise training therapy in clinical practice
and improve quality of life.(5) The drugs are chosen based on the desired effects and patient
tolerance. Our patient is currently taking metoprolol, losartan, furosemide, spironolactone,
hydralazine, Isordil, aspirin and atorvastatin. Metoprolol is a beta blocker and ensures a slow
progression and improves survival. It also acts as antiarrhythmic agent. Carvedilol improves
survival compared to metoprolol. (6) BB should be used cautiously, titrated slowly because they
may initially worsen CHF that’s why we initially had this patients’ metoprolol at 25mg and then
titrated it to 50mg. The standard of care is the angiotensin converting enzyme inhibitor as it
slows progression of left ventricular dysfunction and improves survival. However, the most
common side effect is coughing so we decided to hold ACEI for our patient to alleviate the
coughing. Losartan is an angiotensin receptor blockers (ARB) and is used as second-line to
ACEI if ACEIs are not tolerated, or as adjunct to ACEI if beta blockers are not tolerated. ARB
combination with ACEI is not routinely recommended and should be used with caution as it may
precipitate hyperkalemia, renal failure and the need for dialysis.Combination of angiotensin II
receptor blockers with neprilysin inhibitors is a new class of medication that has morbidity and
mortality benefit over ACE inhibitor alone. This may become standard first line therapy. (7)
Furosemideis a diuretic and is given for symptom control to manage fluid overload and also
oppose the hyperkalemia that can be induced by beta blockers, ACEI, ARBs, and aldosterone
antagonists. Spironolactone is an aldosterone antagonists and it has mortality benefit in
symptomatic heart failure with severely depressed ejection fraction. It is given to symptomatic
heart failure patients already on ACEI, beta blocker and loop diuretic. It can potentially cause life
threatening hyperkalemia and hence the need for monitoring. Hydralazine used in combination
as Isosorbide dinitrate/hydralazine is a vasodilator and is used in heart failure patients
especially of African origin. (8)Isordil is used to relieve chest pain while aspirin is used to
prevent clot formation and atorvastatin to lower the LDL level.
According to current guidelines, cardiac-resynchronization therapy (CRT) is indicated for
patients receiving stable medical therapy recommended by current guidelines who have
moderate-to-severe heart failure, a left ventricular ejection fraction of 35% or less, and a QRS
duration of 120 msec or more as assessed electrocardiographically.(9)Implantable cardioverter–
defibrillators (ICDs) improves survival among patients who have New York Heart Association
(NYHA) class II or III heart failure with left ventricular systolic dysfunction despite optimal
medical therapy. (10) Cardiac transplantation is available for only a minority of patients,
because of a lack of suitable donor hearts. (11)
Despite recent advances, heart failure remains a common cause of death and morbidity.
However, the risk of sudden death has changed over time among patients with symptomatic
heart failure and reduced ejection fraction with the sequential introduction of medications
including angiotensin-converting–enzyme inhibitors, angiotensin-receptor blockers, beta-
blockers, and aldosterone antagonists. (12)
In conclusion, heart failure requires extensive treatment with both pharmacological and
procedural therapies. ARB in combination with neprisilyn inhibitors has proven to be superior to
ACE inhibitors. Carvedilol improves survival compared to metoprolol. Exercise training therapy
in clinical practice will improve quality of life than no exercise at all. Even patients with NYHA
class II or III can receive ICD therapy to improve survival while undergoing optimal medical
therapy.

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