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Case Study

A Case of Inferior & Right Ventricular Infarction
Prof Dr Kasim Chimthanawala
'Camphor / Amyl-nit

The epidemics of cardiovascular disease, especially IHD are emerging in developing countries and the incidence continues to rise. India is no exception. It is estimated that up to three quarters of mortality in developing countries results from various non-communicable diseases and coronary artery disease tops the list of killers, surpassing even infectious diseases.. As a consequence, more and more patients of IHD with their attendant complications are hospitalised and subjected to a battery of investigations.

Pathologically, it is generally accepted that Myocardial Ischemia, and its extreme consequence - acute myocardial infarction, can result from a transient or a permanent disproportion between myocardial oxygen demand and coronary artery blood supply. Ischemic heart diseases can result from encroachment on the coronary artery lumen by disease of the arterial wall (arteritis), intraluminal obstruction (atheroma or embolism), or an excessive increase in myocardial oxygen demand exceeding the ability of the normal coronary arterial system to supply the needed blood (aortic stenosis). Of these, Atherosclerotic Coronary Artery disorders form the major proportion of cases in our Out Patient Department.

When we study the genesis of these disorders, it becomes obvious that the disease spectrum has an evolutionary dimension. It starts from a functional state and ends at an organic level (atherosclerotic plaque) with its attendant secondary symptoms. Earlier it was accepted that the incidence of Myocardial Infarction increases rapidly with age. But today there is an emergence of Coronary artery disorders in the Young (> 40 yrs). The implications of Ischemic Heart Disease in young patients go beyond prognosis, as repercussions on the entire family structure and community commonly ensue with a growing economic and social burden. It is apparent that there is a need to understand better the potential to return to work, the degree of symptoms to be expected vis a vis homoeopathic therapeutics in these patients..

This prompted the National Academy of Homoeopathy, India, to open a separate Homoeopathic Cardiological Cell at its Central Secretariat at Nagpur, where detailed homoeopathic study in this specific area can be undertaken.
Here under, I present one case of Subendocardial Inferior and right Ventricular Infarction from our records.

Ma X, 22y, studying in B Sc, was brought at Shaad at around 2 am on 14/03/02 with:
1. Chest pain - sudden onset, Retrosternal, localized dull aching.
2. Vomiting - twice, consisted of only food, non projectile, No nausea
3. Prostration ++ with cold sweat +
4. Was anxious, restless & persistently wished to sit in spite of having no breathlessness.
5. Disliked being covered (feet & hands were cold).

All complaints developed with increasing intensity within 1-2 hrs, while he was preparing for his exams. No such similar complaints reported in the past. No H/O loose motions, palpitation, vertigo, abdominal pain or other complaints except H/O active bleeding piles since 4 days.

O/E General condition not satisfactory; well built, restless & cold.
Pulse-Reg 130/min, synchronous, low volume
BP 90/60 mm Hg, No Oedema feet, JVP - Not raised but HJR positive.
No pallor/Icterus/clubbing; Central Cyanosis+. Face pale, cold with profuse sweat all over,
CVS-HS 1st muffled, P2 loud, No S3 gallop
RS-RR 28/min thoraco-abdominal, Breath Sounds Vesicular. No Rales.
PA - soft, Non-tender, Liver /Spleen- Not Palpable, Kidneys-not ballotable, No E/o Ascitis, sounds+
PR - Grade 2 Haemorrhoids ++. CNS-NAD

On this clinical presentation, Pt was hospitalised in the ICCU. Taking his age into consideration, a possibility of Severe Gastritis/ Oesophagitis/ Acute Pancreatitis and Angina were considered. An ECG established the diagnosis Acute Inferior Wall with Right Ventricular Subendocardial Infarct with Early Right Ventricular Failure with Hypotension. Carbo-veg, Cactus, Aconite and Actea were considered but the symptom totality pointed towards Camphor

2.10 am

ECG-ST depression (2mm) II, AvF, (4mm) rV4 with T inversion sinus tachycardia

Camphor 30 x 10 min
POPosition, O2 inhalation
Amyl-nitr Q 
nebulizer ½ h
IV DNS (dose titrated)

2 hrs after

Pt quiet, restlessness >, chest pain>>, Heavy feeling chest ++, passed urine 50 cc, Afebrile, P-110/m, BP 100/64

Camphor 30 x 2 hrs
O2/Amyl-nitr SOS

10 am

GC fair, Pt settled, Troponin T+, S CPKMB -47 I U/L, SGOT-56U/L, urea-32 mg/dl. S, Cr 1.4 mg/dl

Ct same
Ct. Ringer Lactate

4 pm

Restlessness, prostration >, No vomit, No cyanosis. BP 110/70 mmHg, Electrolytes-WNL

Omit Amy-nit
Rest Ct all

9.10 pm

Retrosternal Chest pain relapsed < lying had to sit x 5 min, feeling of weakness++, restlessness +++, BP 80 mm Hg Systolic, No Fresh ECG changes

IV NS@ 20 Dr/min
200 Fract Ds

11.30 pm

Chest pain >, restlessness +, P-100/mm Hg, BP 100/70 mmHg

Ct all

Next day

Pt >, did not sleep well, No chest pain, dyspnoea Palpitation, Vomiting Urine 800 cc/24 hrs, P 100/min, Reg; BP 114/80 mm, JVP-NR ECG-IWM1 (Non Q wave)

Sac lac x 1 hrly
Omit IV fluids
Light diet

16 March

ECG-IWM1 (Non Q wave)
Sleep>, GC fair, Chest pain >>, Passed soft stool 5 am, Urine

Sac lac TDS

17 March

1150/24 hrs, Vitals stable, ECG-WNL
GC fair, no major comp, P-86/m, Reg; BP 120/76, ECG -

Sac lac TDS

18 March

WNL. Lipid profile-N
Patient>>, Stool/Urine N, Vital Stable, BP 110/80, RS-clear

Discharged on request
BD x 7 days

22 March

HS pure, Adv ECHO/Coronary Angiography
2D ECHO-Normal

SL BD x 15 days

1 mth after

Follow-up: No complaints

Arg Nit 1M 1D


Detailed life history
All Complaints much >>,


 was administered on the basis of exhaustion, debility, sudden onset Restlessness, Anxious, SIT INCLINATION to, Central Cyanosis, Face pale, cold with profuse sweat all over, did not want to be covered; {Combined & Synthesis Repertories}Camph was started in low potency. Kent says: In the mental state there is anxiety and extreme fear; fear of persons, of the dark, the patient is most troublesome patient to nurse; nobody and nothing suits. He cannot endure covering to warm his limbs though he suffers from cold. Robin Murphy gives the following Modalities.
> free discharges, sweat, thinking of it, drinking cold water.
< motion, night, contact, cold air, when half asleep, mental exertion,

 covered the acute case totality so much so that only once after admission did he get an anginal attack with sudden hypotension. Of course since his lipid profile and coronary angiogram was normal which is a usual finding with young patients of Myocardial infarction - the basic pathologic mechanism for this attack was not atherosclerosis but a severe coronary vaso-spasm leading to an infarct (a functional manifestation indeed). This patient was given Arg-nit 1M 1 dose which was his constitutional remedy, to remove the hyper-irritability of the smooth muscles of the arterial wall.

2.) Amyl-nit 
nebulization was given concurrently for oppression of chest. Even IV fluids were extremely important because Inferior and Right Ventricular infarction pts generally present with vomiting, since the Inf. Wall is close to the stomach and sudden hypotension due to over action of vagus nerves.