Introduction
Cardiovascular
disease constitutes the recurrent dominant cause of universal death affecting
the youthful society. (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 kidney disease predictions on clinical
practice guidelines proves the demonstration of ischemic chest pain is a strong
venue of cardiovascular morbidity measures and all cause-mortality (3) with classifications
of hemo- dynamic alterations independently calculate glomerular filtration rate
(eGFR) on the scheme of arbitrary renal
staging in altering albuminuria, hyperfiltration and hyperglycemia in renal
failure. Consequently CKD as a clinical syndrome equivalent to CHD investigate
the urinary excretion proteins and TGF-beta 1 initially in nephropathy as a
diagnostic value in clinical parameters of previous MI in diabetic individuals. (4)
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In the
Framingham heart study, the estimation of silent ischemia detection on large
scale misinterpret by atypical angina following normal ECG with the
unnoticeable prevalence in broad ranging population <45years young men and
women including the illness of metabolic impairments, eGFR fall, advanced CKD
at dialysis, chronic inflammations and prothrombic attributes in the acceptable
autopsy reports.(5) Additionally diabetic kidney
disease progress with the albuminuria status and serum creatinine measurements on screening at initial
conventional method in pubertal diabetic interval challenging hyperglycemia on
clinical nephropathy.(6)
According
to the Epidemiological controversies, poor estimation of CAD in CKD cases at
less ratios make the diagnostic differences by the interpretation of ECG
changes, risk factor profiles, pain perception, cardiac biomarkers and MI
perfusions assessment in the objective of angina culminate the presentation of
constant changes in troponin values represent the attributes of premature CHD
by the conclusion of progressive atheromatous plaques and calcifications on the
likelihood of sepsis, anemia, platelet aggressiveness, nitric oxide abnormal
metabolism, arterial stiffness, calcium-phosphate homeostasis, endothelial
dysfunctions, recreational drugs, history of multiple traumas and surgeries. Classically,
we present the case of inferior MI in young women with type 2 diabetes
evolutions of 10 years and previous heart failure cause to death prolonging the
complications of dyslipidemia progressive to the advancement of diabetic
nephropathy in extending membranoproliferative glomerulonephritis.
Case presentation
A 35
year old female present to Emergency Department 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 in 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, Cardiac sounds were normal on 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 diagnosis begin with the measurement of cardiac
enzymes 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 LVEF of
48% motion index on homogenous contrast reflecting MI tension on inferior wall
suspecting intracardiac thrombosis and 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 Diagnosis
Prinzmetal
s angina/vasospasm, cardiogenic shock, cardiac contusion, pulmonary edema,
acute gastritis, GERD and anxiety disorders are unlikely considered on pursued
clinical presentation as reviewd.
Treatment
Management
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 up
On 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