According To Aha & AccL:

Cardiac arrest is the abrupt loss of heart function in a person who may or may not have been diagnosed with heart disease. It can come on suddenly, or in the wake of other symptoms. Cardiac arrest is often fatal, if appropriate steps aren’t taken immediately.

According To Braunwald:

Sudden cardiac death (SCD) is natural death due to cardiac causes, heralded by abrupt loss of consciousness within 1 hour of the onset of acute symptoms.

Preexisting heart disease may or may not have been known to be present, but the time and mode of death are unexpected.

Cause of Cardiac Arrest:

Coronary Artery Abnormalities:

• Coronary atherosclerosis
• Chronic ischemic heart disease with transient supply-demand imbalance thrombosis, spasm, physical stress
• Acute myocardial infarction
• Chronic atherosclerosis with change in myocardial substrate.

 Congenital abnormalities of coronary arteries.

 Congenital abnormalities of coronary arteries.

Congenital Abnormalities of Coronary Arteries

 Anomalous origin from pulmonary artery

• Other coronary arteriovenous fistula
• Origin of left coronary artery from right sinus of Valsalva
• Origin of right coronary artery from left sinus of Valsalva
• Hypoplastic or aplastic coronary arteries
• Coronary-intra cardiac shunt.

Coronary Artery Embo Lism

• Aortic or mitral endocarditis
• Prosthetic aortic or mitral valves
• Abnormal native valves or left ventricular mural thrombus
• Platelet embolism.

Coronary Arteritis

• Polyarteritis nodosa, progressive systemic sclerosis, giant cell arteritis
• Mucocutaneous lymph node syndrome (Kawasaki disease)
• Syphilitic coronary ostial stenosis.

Miscellaneous Mechanical Obstruction of Coronary Arteries

• Coronary artery dissection in Marfan's syndrome
• Coronary artery dissection in pregnancy
• Prolapse of aortic valve myxomatous polyps into coronary ostia
• Dissection or rupture of sinus of Valsalva.

Functional Obstruction of Coronary Arteries

• Coronary artery spasm with or without atherosclerosis
• Myocardial bridges.

Hypertrophy of Ventricular Myocardium

• Left ventricular hypertrophy associated with coronary heart disease
• Hypertensive heart disease without significant coronary atherosclerosis Hypertrophic myocardium secondary to valvular heart disease.

Hypertrophic Cardiomyopathy

• Obstructive
• Nonobstructive.

Primary or Secondary Pulmonary Hypertension

• Advanced chronic right ventricular overload
• Pulmonary hypertension in pregnancy (highest risk peripartum).

Myocardial Diseases and Heart Failure

• Chronic congestive heart failure
• Ischemic cardiomyopathy
• Idiopathic congestive cardiomyopathy
• Alcoholic cardiomyopathy
• Hypertensive cardiomyopathy
• Post-myocarditis cardiomyopathy
• Postpartum cardiomyopathy.

Acute Cardiac Failure

• Massive acute myocardial infarction
• Acute myocarditis
• Acute alcoholic cardiac dysfunction
• Ball-valve embolism in aortic stenosis or prosthesis.

Mechanical Disruptions of Cardiac Structures

• Rupture of ventricular free wall
• Disruption of mitral apparatus
• Papillary muscle
• Chordae tendineae Leaflet
• Rupture of interventricular septum
• Acute pulmonary edema in noncompliant ventricles.

Inflammatory, Infiltrative, Neoplastic, and Degenerative Processes

• Viral myocarditis, with or without ventricular dysfunction
• Acute phase
• Postmyocarditis interstitial fibrosis
• Myocarditis associated with the vasculitides
• Sarcoidosis
• Progressive systemic sclerosis
• Amyloidosis
• Hemochromatosis
• Idiopathic giant cell myocarditis Chagas’ disease
• Cardiac ganglionitis
• Arrhythmogenic right ventricular dysplasia; right ventricular cardiomyopathy
• Neuromuscular diseases (e.g., muscular dystrophy, Friedreich's ataxia, myotonic dystrophy.

After viewing detail cause factor of sudden cardiac arrest the major cause of SCD is coronary artery disease in hereditary.so a gene 9p21 locus associated with a ~30% increased risk of CAD per copy of the risk allele. Evidence suggests that the 9p21 risk variants alter expression of the noncoding RNA ANRIL, thereby altering activity of two nearby cyclin dependent kinase inhibitors (CDKN2A and CDKN2B) involved in regulation of the cell cycle and cellular proliferation. Furthermore, inflammatory signaling mediated by interferon-γ may alter long-range DNA interactions, linking the 9p21 risk alleles to CKDN2A and CDNK2B expression. This all thing is happen clinically asymptomatically in the fetal life the role of this 9p21 can some time cause a disease called Catecholaminergic polymorphic ventricular tachycardia (CPVT) but if this disease is not establish in the patient then the definitely the patient develop cardiac arrest in the future CPVT can only develop when the father is having same carrier allele at same locus. It means that both parents have disease allele in 9p21.Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a pathological condition in which a ventricular arrhythmia may be triggered by intense physical exercise or acute emotional stress. Typical clinical manifestations of CPVT include dizziness and syncope. However, ventricular arrhythmia may degenerate into rapid polymorphic ventricular tachycardia and ventricular fibrillation, leading to SCD. Since individuals with CPVT have normal resting electrocardiograms, diagnosis may be difficult. CPVT is characterized by both autosomal dominant and autosomal recessive (less frequent) patterns of inheritance. CPVT is caused by mutations in genes encoding ion channels or calcium-handling proteins that primarily affect the electrical activity of the heart. In particular, the first genetic alteration associated with CPVT was identified in the RYR2 gene. After seeing this the mechanism of sudden cardiac arrest is basically genetic basis only one the thing is that if first degree blood relative of any one parent or both parent have this disease then chances of this to the developing baby is increase from 50% to 75%

So the mechanism to cause cardiac arrest is divide into three major heart disease

• CPVT- in children up to 15 years of age
• Ventricular fibrillation.Figure 1: Electrical conduction system of the heart is affected.

  Out these three disease condition electrical mechanical disjunction of heart is the key role factor for cardiac arrest because this disease is associated withvoltage gated ion channel of heart these voltage gated ion channel become imbalance during cardiac arrest the flow of sodium potassium and calcium is affected.

  Cardiac muscle has some similarities to neurons and skeletal muscle, as well as important unique properties. Like a neuron, a given myocardial cell has a negative membrane potential when at rest. Stimulation above a threshold value induces the opening of voltage-gated ion channels and a flood of cations into the cell. The positively charged ions entering the cell cause the depolarization characteristic of an action potential. Like skeletal muscle, depolarization causes the opening of voltage gated calcium channels and release of Ca2+ from the t-tubules. This influx of calcium causes calcium-induced calcium release from the sarcoplasmic reticulum, and free Ca2+ causes muscle contraction. After a delay, potassium channels reopen, and the resulting flow of K+ out of the cell causes repolarization to the resting state. There are important physiological differences between nodal cells and ventricular cells; the specific differences in ion channels and mechanisms of polarization give rise to unique properties of SA node cells, most important, the spontaneous depolarizations necessary for the SA node's pacemaker activity.

Cumin has various genotype RZ-19, RZ-223, RZ-341 and RZ345 were collected from Agricultural Research Station Mandor Jodhpur. The essential oil was extracted using hydro-distillation (HD) in Clevenger-type apparatus. Hundred gram powdered sample was used to essential oil extraction. RZ-19, RZ-223 are most important genotype after fusing them we get the desire property that is they maintain the this voltage gated ion channel in the heat and reduce the risk of cardiac arrest The composition is given by oral route and it is given in early age because during pregnancy if we take the detail family history of the patient we easily understand that there is chance of cardiac arrest is there or not if yes then person should have definitive a pre hypertensive nature so we have to monitor and if we do 2-dimensional echocardiogram of them we can see that there is fast heart beat and these have also have increase in troponin level but these increase is slightly in early stage and there pulse is also very rapid with uniform symmetry but irregular pattern So this composition is given so that it will decrease the risk of cardiac arrest with regular monitoring at regular interval of 3 month and it should be given in prescribed amount.

Buchanania Lanzan Role in Cure of Coronary Artery Disease

Defination:

• Atherosclerosis is a disease in which plaque builds up inside the arteries.
• Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Over time, plaque hardens and narrow the arteries. This limits the flow of oxygen-rich blood to the organs and other parts of the body.
• Atherosclerosis can lead to serious problems, including heart attack, stroke or even death.

  According To Aha:

  • Atherosclerosis is a slow, progressive disease that may start in childhood. In some people, atherosclerosis progresses rapidly in their 30s. In others, it doesn’t become dangerous until they reach their 50s or 60s. (Some hardening of the arteries is normal as people age.)
  • Exactly how atherosclerosis starts or what causes it isn’t known.

  How These Plaque Occur In Artery:

  Early fatty streak development begins in childhood and adolescence. The initial step occurs when LDL particles leave the blood and enter the arterial intima, where LDL levels are increased, they accumulate. They then are modified by enzymes and are oxidized into pro inflammatory particles which provoke the reaction of the innate inflammatory system within the intima. Fat droplets may accumulate in the cytoplasm of smooth muscle cells. These first changes in the arterial wall occur at the branch points of arteries, where adaptive intimal thickening occurs in response to normal hemodynamic stresses. Inflammation begins when the endothelial cells become activated and secrete adhesion molecules, and the smooth muscle cells secrete chemokines and chemoattractants, which together draw monocytes, lymphocytes, mast cells, and neutrophils into the arterial wall. Intimal smooth muscle cells also secrete into the extracellular matrix proteoglycans, collagen, and elastic fibers. Upon entry, monocytes transform into macrophages, take up lipids as multiple small inclusions, and become foam cells. The degree of lipid accumulation is critical for early-stage diagnosis of atherosclerosis. Isolated foam cells, multiple layers of foam cells, and isolated extracellular pools of lipid are not considered atherosclerosis. These early changes are microscopic and may progress to gross visibility. These lipid changes can be reversed. Atherosclerosis is believed to start when the lipid accumulation appears as confluent extracellular lipid pools and extracellular lipid cores with decreased cellular it.

  Dissolve the Plaque

  The plaque should be dissolved with very less side effect if the chemical compound taken by the patient for long time then also it should have less side effect.

  Buchanania lanzan is a deciduous tree which produces seeds that are edible to humans. It is known as Chironji. These almond- flavored seeds are used as a cooking spice primarily in India. Buchanania lanzan is cultivated across India, primarily in the northwest.

  Origin and Distribution

  • This is basically found in north, west and central India
  • Plants may be seen in the forest of Uttar Pradesh, Madhya Pradesh, Chhattisgarh Bihar, Jharkhand Orissa, Andhra Pradesh, Gujarat and some parts of Rajasthan.

  Important Genotype

  • CPT -1
  • CPT-7
  • CPT-33
  • CPT-32
  • CPT-2                these two genotype are highly important
  • CPT-40

  CPT – 2

  • Found in Gujarat
  • Fruit weight - 1.314g by gene 21
  • Total soluble solid - 21.21% by gene 22
  • Total sugar - 14.40% by gene 25
  • Vitamin –c - 46.50mg/100g of stone weight 0.55g by gene 23
  • Kernel weight - 0.13g by gene 24
  • Kernel protein - 30.70% gene27

  CPT – 40

  • Found extensively in Chhota Udaipur of Rajasthan
  • Fruit weight – 0.05g by gene 15
  • Total soluble solid - 23.00% gene 19
  • Total sugar - 15.00 % gene 14
  • Vitamin –c - 50.00 per 100g of stone weight 0.42g gene 16
  • Kernel weight - 0.42g gene 12
  • Kernel protein - 30.10% gene 13 vitamin k2 28.30% by gene 17.

    Crossing Over

    Now we cross these two genotype i.e. CPT-2 AND CPT-40 Selecting only those gene which we need i.e. gene of kernel protein vitamin c and vitamin k Now this hybrid variety of chirongi consist high kernel protein and vitamin enriched content The route of administration of drug is same as of statins But the main point of difference in this that the statins act on the upper part of Mevalonate cycle and this hybrid act on lower part of cycle Because statins act on upper part is contain certain side effect.

    Side Effect of Statins

    • The most important adverse side effects are muscle problems
    • An increased risk of diabetes mellitus
    • Increased liver enzymes in the blood due to liver damage.
    • Other adverse effects include neuropathy
    • Pancreatic and liver dysfunction
    • Statins act by competitively inhibiting HMG-CoA reductase, the rate-limiting enzyme of the mevalonate pathway. Because statins are similar in structure to HMG-CoA on a molecular level, they will fit into the enzyme's active site and compete with the native substrate (HMG-CoA). This competition reduces the rate by which HMG-CoA reductase is able to produce mevalonate, the next molecule in the cascade that eventually produces cholesterol.Cause of Side Effect
      • No doubt that statins stop or decrease the formation of LDL in body but the major cause of side effect is Coenzyme Q10 which is an important vitamin-like substance required for the proper function of many organs and chemical reactions in the body. It helps provide energy to cells.
      • Coenzyme Q10 also seems to have antioxidant activity. People with certain diseases, such as heart failure, high blood pressure, gum disease, Parkinson's disease, blood infections, certain diseases of the muscles, and HIV infection, might have lower levels of coenzyme Q10.
      • Coenzyme Q10 is present in the membrane of mitochondria. When statins acting on mevalonate pathway it also suppress the formation of this co enzyme however if the drug is given in the lower mevalonate pathway then it will not suppress the formation of co enzyme Q 10.

      At Molecular Level:

      • These statins act on upper part of mevalonate cycle because at molecular level the structure of statins is similar to the structure of HMG – COA and in place of HMG – COA these statins bind to the receptor.

      At Molecular Level:

      • After performing many molecular examination by certain agriculture institute of INDIA and ISRALE they also put there report. That Buchanania lanzan is biocompatible and helpful to human kind.
      • From these report I observe is that after seeing spectroscopic and radiologic images that at molecular level of Buchanania lanzan (chirongi) is having similar structure to mevalonate -5- phosphate decarboxylase enzyme.
      • Now this drug given to the patient then we control level of LDL in the body.
      • And in this stage it does not suppress the coenzyme Q10 and does not show any kind of major side effect after giving for prolonged period of time.Contra Indication
        • Cannot given to a patient suffering from asthma and liver cirrhosis.
        • Patient suffering from portal hypertension.
        • Patient suffering from jaundice.
        • Patient suffering from renal problem.
        • From the above contraindication then we need to give chirongi along with beta blocker will be given as this combination will definitely help the patient in atherosclerosis.

1. Almeida MR. Buchanania cochinchinensis. 1996; 1: 287.
2. Spreng BL. India Biodiversity Portal. 2017; 12: 5.
3. Jump up to a b Celtnet Spice Guide Engtry for Chironji Celtnet Spice Guide. August 11: 2012.
4. Jump up to a b c Bowen Dana. TEMPTATION Charoli Nuts Flavor the Dishes and Memories of Indian Chefs. New York Times. April 17, 2010.
5. Oudhia P, Robert E. and Paull. Chironji Buchanania lanzan Spreng Anacardiaceae Encyclopedia of Fruit and Nuts. United Kingdom. 2008; 14-15.
6. Chironji (Buchanania lanzan) fruit juice extraction using cellulase enzyme modelling and optimization of process by artificial neural network and response surface methodology.
7. Dileswar Pradhan S. Abdullah and Rama Chandra Pradhan.