IntroductionCardiovascular
disease constitutes the recurrent dominant leading cause affecting the young
population in global health worldwide. (1) The
clinical entity silent MI annually experience CHD with the approximate 9.8
million every year predicting the unrecognized symptoms related with the phenomenon
of either ambulatory ischemic events or unexpected death on 70%-80%  asymptomatic manifestation.(2) The substantial long standing kidney disease
outcomes on clinical guidelines approved the theory of ischemic chest pain
demonstrate the strong venue of cardiovascular morbidity measurements at all
cause-mortality (3)  with grading of  independent hemodynamic estimations in
calculating eGFR rate on the arbitrary scheme of renal failure in the
alterations of albuminuria, glycemia and glomerular filtration. Clinically CHD
equivalent to CKD as a consequent syndrome initially investigate the excretory
proteins and TGF-beta 1 as a diagnostic value in diabetic nephropathy
individuals on clinical parameters of previous MI. (4) In the
Framingham heart study, the classification of large scale interpretation
following the detection of  atypical
angina with broadly ranging of  unnoticeable normal ECG prevalence in the
extended population of <30years young men and women including the illness of metabolic impairments, eGFR decline, chronic  inflammations, hypercoagulability and the kidney dialysis complications arethe attributes on the acceptable autopsy reports.(5) Additionally pubertal diabetic kidney disease progression screen the albuminuria and serum creatinine status at conventional method challenging the clinical interval of hyperglycemia in nephropathy.(6) The Epidemiological controversies accordingly estimate the poor risk ratio of CKD cases in CAD by making the diagnostic differences of  sepsis, anemia, platelet aggressiveness, nitric oxide abnormal metabolism, arterial stiffness, calcium-phosphate balance, endothelial dysfunctions, recreational drugs, history of multiple traumatic surgeries can culminate in the objective assessment of constant troponin value changes, pain recognition, risk factor profiles and the MI reperfusions conclude the premature CHD on the likelihood of atheromatous plaques and calcification progression. Classically, we present the instance of STEMI in young patient with type 2 diabetes evolutions of 10 years prolong the risk of dyslipidemia complications to death accelerating the progression of nephropathy advancing in the membranoproliferative glomerulonephritis.Case presentationA 35 year old female present to Emergency ward with severe chest pain, palpitation and vomiting for 3 days. She has been diagnosed with the previous episodes of heart failure and traditional risk factors of CAD at medical history. She described her chest pain with tightedness and flank dull pain at both the areas of kidneys with back pain.On physical examination, Heart murmur sounds are normal on cardiac auscultation with no tenderness on palpation, no intra-abdominal rebound masses, no neck stiffness, no jugular vein enlargement, no dysmenorrhea, no clubbing, no family history of CAD and no hypertension. She was profound sweating on presence with weight loss, urine retention, fatigability and restlessness from 1 week. Her medications at the time of review include Aspirin, Statin, Metformin, Insulin, Diuretics and Omeprazole.  At Admission, BP was 85/60mmHg and her heart rates 66 bpm. ECG showed normal sinus rhythm with ST elevation in leads II, III and avf with the reciprocal of ST segment depression in leads V1-V6 as shown in Fig 1A The crucial step for ruling out myocardial injury, clinical diagnostic begin by the measures of cardiac enzymes level as shown in Table 1 Moreover on the primary assessment of troponin elevation and NT-proBNP impairment assess the specificity and sensitivity limitations on trans-thoracic echocardiography revealing hypokinesia with an reduced LVEF  of 48% homogenous contrast reflecting MI tension at inferior wall suspecting intracardiac thrombus or pulmonary embolism.Figure 1 (A) Initially ECG shows ST elevation at inferior leads with the reciprocal of ST depression in avR.               (B) No simultaneous changes in right ventricular MI on various segments of ECG.               (C) New ST depression in the leads of II. III , and avF after following fibrinolysis in 12 lead ECG. Table 1 Clinical values of Combined Detection of 5 Indicators in the Diagnosis of Acute MI. In the suspection of fibrinolysis and thrombo embolism, thoracic ultrasonography TUS certainly performed prior to the normal chest imaging previously and false positive predictive value in D-dimer test as shown in Table 2 On the emergency based history of angina, bilateral thoracic probe examine the presence of the left sided non specific pleural lesion of more than 5mm on screening. It provokes the follow up of thrombolytic with the association of hypotension. Therefore, anticoagulation includes low-molecular- weight heparin therapy (LMWH) and tPA produce successful reperfusion within 12hrs non-invasively.Table 2 Quantitative D-dimer Assay for Pulmonary Embolism Diagnostic Test. In regards with Gastrointestinal aspects, the alarming signs of dehydration, nausea, vomiting, fatigue and back pain warrant the examination of a comprehensive metabolic panel and amylase, lipase testing for the consideration of gastroenteritis or acute pancreatitis. The normal values result self-limiting bacterial infections by the management of fluid replacement, Calcitonin and supportive care.As the patient on type 2 diabetes expansion on clinical estimation follow urinalysis on palpation of the bladder and oliguria. According to the quantitative measurements on total protein positive test, the exercising ECG reviewed on high standards verify the reciprocal changes in pathologic Q waves and hyper acute T waves in nonfatal angina attack reflect preload independently as shown in figure 1B Apart from the renal profile, further globulin tests were progressed on the basis of laboratory evidences as shown in Table 3 – 4 decline in eGFR, leucocytosis and elevated cholesterol conclude the pathogenesis of contrast induced nephropathy in association of nephrotoxic drugs eliminating the advanced staging of kidney damage other than glomerulonephritis and residual renal dysfunctions.Table 3 Comprehensive Metabolic Panel with eGFR Blood Test. Table 4 Complete Blood Count Test Results. On the basis of ANA negative investigation, monoclonal immunoglobulin IgG determine the pre-malignancy in renal insufficiency with plasmapheresis at high risk of multiple myelomas as shown in Table 5 here in the diagnosis of proteinuria and myeloma related diseases Bence Jones test reveal false negative results in concentrated urine. At result, vitamin K status in CKD sub clinically link to the formation of arterial calcification in the high moderations of atherosclerosis constitute the notable limitations on independent peritoneal dialysis to maintain the equivalent nutrition at the less co-morbidity of young age in CKD.Table 5 Serum Protein Electrophoresis to diagnose M protein. Differential DiagnosisPrinzmetal s angina/vasospasm, cardiogenic shock, cardiac contusion, pulmonary edema, acute gastritis, GERD and anxiety disorders are unlikely considered on pursued clinical presentation as reviewd. TreatmentManagement is initiative with the long-lasting insulin therapy in type 2 diabetes with the combination of Sulfonylurea and Metformin to control hyperglycemia. Secondly use of diuretics to restore electrolyte imbalance and Vitamin C for the nauseate feeling. Thirdly Diazepam orally for the anxiety and cardiac therapy Cedilanid for hemodynamic stability, Dopamine hydrochloride for improving the cardiac functions, Hydroxylamine and MgSO4 to control frequent arrhythmias, Clopidogrel 150mg + Aspirin 100mg with heparin therapy of LMWH in the preventions of heart failure and recurrent myocardial infarction. Lastly IV Sodium bicarbonate+ insulin+ 50% Dextrose for hyperkalemia and Atorvastatin of 20mg oral/day for LDL reduction.Follow upOn the Ninth day, ECG changes as shown in fig 1C, ST resolution and T wave inversion after the pharmaceutical drugs. At practical measures IV human albumin infusion as a therapeutic plasmapheresis remarkably improved the tailored indication of hypovolemic shock in the significance of cardiac improvement. Hence at the objective of primary care with proper monitoring of stable renal functions by calcium gluconate, on fifteenth day patient discharged with effective diet planning assumed by community-based clinicians in providing self management to control delicate balance in postprandial hyperglycemia adjustments.  Discussion  The DIAD (Ischemia detection in asymptomatic Diabetics)  (5, 7) assumes the importance of greater incidence in long standing type 2 diabetes mellitus focus on the factor of occlusion in arteries on the possibility of judicious analyses with no support of scientific data in the management of anti-ischemic medications at frequent CAD cases. Hence, the investigations of massive consequences intermediate undoubtedly on clinical scoring as addressed for the issue of positive prognostic screening program in the upcoming studies. American Diabetes Association (ADA) recommend the measures of Beta blockers or re-vascularization medical therapy on aggressive intensive treated cases on investigating the annual review of abnormal resting ECG with the lesser degrees of ischemia intervention can improve the prognosis on cardiovascular events. The nontraditional factors of hyper coagulation and clotting mediators (8) pronounce the elevation of high risk on thrombic events statistically with the complications of CKD underlying the unclear etiology predominantly result congestive heart failure, ESRD, hemorrhagic stroke and relative risk of peripheral artery disease proportional to sudden cardiac death. Thus, an appropriate medical therapeutic management needed in terms of risk factors incidental preventions in adult onset diabetes. (9)  In primary prevention study at Helsinki Heart Study (10) show poor outcomes in Diabetic individuals with CHD identifying high risk of aggressiveness in dyslipidemia treatment for the maintenance of LDL and Total protein target the statin drugs as a pharmacological intervention for the trials as a first choice in young diabetic nephropathy patients. The General Practice Research thrombosis Prevention trial (11) on the  secondary prevention confirm the benefit of Aspirin treatment in the establishment of atherosclerotic disease in prospective trials reduced the risk of CHD and non fatal events on the clinical recommendation of anti-platelet therapy can also be used as a preventive strategy to overt the nephropathy in <30 years age individuals. Therefore large phase prospective studies and trials are required to explain the issues of uncertain protein restriction in the adherence of management in routine setting care in diabetic nephropathy.  Observational Studies in the demonstration of direct effect on CVD risk factors deteriorate the kidney functions in hyperglycemia. The Reduction of End points in Non-insulin-dependent Diabetes with the Angiotensin II Antagonist Losartan (RENAAL) and Irbesartan Diabetic Nephropathy Trial (IDNT) studies include the trial of Losartan and Iresartan as a renoprotective in the combination of Ramipril and Telmisartan initiate the defensive effect on proteinuria as compared to the therapy of (VA NEPHRON-D) study of Losartan and Lisinopril on macroalbuminuria >300mg/day. Thus, the supportive directions on definite
limitations of safety concerns utilize the consideration of Renin Angiotensin
Aldosteron System (RAAS) lessens micoalbuminuria 30-300mg/day in normic
diabetes cases. (12)  Hyperglycemia
as a therapeutic potent in diabetes, the epidemiological early analysis
illustrate the fundamental controversy of minimal outcomes in macrovascular
hazards can ascend the occasion of CVD risk factors, extravagant mortality
rates and vigorous symptoms with the median of HbA1c%. The Action in Controlling
Cardiac Risk factors in Diabetes (ACCORD) present the current affirmation of
delaying vascular complications related to the consequences of CKD staging 3-4
can be patently achieved by the optimal goal of HbA1c and hypoglycemia
incidents. Accordingly, a tight control on hyperglycemia is permeable to
convert the high risk of hyperfiltration and glomerular hypertrophy partially
on HbA1c <7% and apparent supremacy to control the normal ranges with the treatment of insulin in the maintenance of proteinuria on reduced value.   According to the American Heart Association guidelines, the pharmacotherapy in CKD associated with CVD risk factors include the counsel use of Fibrinolytic, Antiplatelet, Glycoprotein II b/III a receptor antagonist, Anti-coagulants, Beta blockers, ACEIs/ARBs, Aldosterone blocker and Statin can assess the randomized controlled trials of efficacy and welfare to diminish the vascular events in non chronic dialysis patients. The another Study of Heart and Renal Protection (SHARP) involve the substantial results in combined therapy composite to the dominance in controlling the major atherosclerotic relative risks, intracranial hemorrhage, left ventricular hypertrophy and STEMI intimated the remarkable decline in hospital death and sudden cardiac arrest for least 1 year. Ultimately, pharmacokinetic studies in renal dysfunction require essential regulations for the clinical controlled trials further on extensive population with distinct precise dosing in terminating the predictable adverse outcome pathways.Learning points·         STEMI feature exceeding QRS height in the form of concave ST elevation.·         Antihypertensive as a binary therapy of ACEI and ARBs are used in supremacy of BP and albuminuria.·         Combined therapy with oral insulin agents should be sustained with HbA1c <7%·         Importance of anti-ischemic and anti-thrombic therapy must be understood as a conservative strategy in <40 age with vascular disease, diabetes and STEMI·         Early screening detection in the initiative of type 2 diabetes kidney related complications.  ·         Determined lifestyle remodeling guidance is paramount in cardiovascular risk factors.