CDSS (conversational): A cardiology intervention (AICD or CRTD) backed by guidlines: Biased evidences
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This is a case of a 63-year-old gentleman who had undergone a balloon surgery in 1993 followed by coronary stenting in 2001 and CABG in 2009. Recently, he has been advised to implant AICD or CRTD. His list of medicines and previous reports and discharge summaries are attached below:
Discharge summary after CABG in 2009:
Coronary angiography in 2009:
Coronary angiography in 2012:
Echocardiography report in 2017:
Below are the recent case story and recent reports few months after the intial tests in 2017
This patient again admitted to the hospital with the history of sudden onset abdominal pain (mainly in epigastric and periumbilical region) for 4-5 days, associated with mild chest pain and bloating sensation and diagnosed to have mild acute pancreatitis and ischemic dilated cardiomyopathy (LVEF 27%).
Recent reports and discharge summary are attached below: Conversations around this:
WhatsApp Conversations around shortlisting essential medications for this patient:
CA 1: This patient again admitted to the hospital with the history of sudden onset abdominal pain (mainly in epigastric and periumbilical region) for 4-5 days, associated with mild chest pain and bloating sensation and diagnosed to have mild acute pancreatitis and ischemic dilated cardiomyopathy (LVEF 27%). http://bmjcaselogvivek.blogspot.com/2017/09/a-63-year-old-male-recieved-ballon.html?m=1
CA 2 (The Patient): "Now I am fine.My cardiac doc suggested some costly medicine for kidney.My ct scan says my kidney is normal.Your adv required and proper medicine to be taken as per my last report."
CA 3: can we put our heads together and optimize his long list of medicines and per efficacy to suit his current requirements?
CA 1: Yes Sir. Let me look into his current prescriptions.
CA 2: I have not started with 3 & 6.No 3 is a kidney medicine and very costly. These 2 medicines r included on 1.12.2017. As per my ct scan my kidney is fine I suppose.May i know your openion about other medicines.Any remedy to improve my health condition.
CA 3: Why is he on thyrox 25? Biochemical hypothyroidism? What was his last thyroid profile? Does flavedon have any efficacy? Does he have any angina symptoms? If his angina is not persistent he may not require long acting nitrocontin but should do OK with sublingual gtn? Ketosteril may not have much evidence for renal protection as much as flavedon doesn't for cardioprotection. Not sure what is the role of nodosis. The list is exhausting. Vivek help with the rest. Most of the medications seem to be overkill?
CA 1: He doesn't have recent TSH done, but his last TSH was 3.33 m IU/L
CA 3: Was on thyrox before that? What was his first TSH?
CA 1: As on 23.8.17 serum tsh was 3.33 and It was 10.10 as on 26.4.17. He started taking thyroxin 25 after that 10.10
CA 3: Alright let him continue that 25 mcg then
Personal communication between the patient Vivek:
CA 1 (To patient): Hello, good morning. We have been discussing one by one all the medications on your list, you can continue thyrox 25 with the same dose. And for other medicines, I will ask time to time your symptoms. Do you have any chest discomfort or chest pain or any exertional chest discomfort or shortness of breath?
CA 2 (The Patient): Recently no.Sometimes I feel bit pressure at chest.Thats all.
CA 3: Thanks for his intermittent symptoms sorbitrate SOS should be good enough
CA 1: Shall I then advise him to stop Flavedon and start Sorbitrate SOS only?
CA 3: What about his other medications?
CA 1: Will discuss that too. Need to discuss the remaining medicines by today.
CA 3: Let's
CA 1: Nodosis tablet 500 mg has been prescribed- Sodium Bicarbonate. I am not sure why was it indicated? Primarily used for "Acidity, Intestinal ulcers, Stomach ulcers" https://www.1mg.com/drugs/nodosis-500mg-tablet-328152#1
We are talking about this patient: http://bmjcaselogvivek.blogspot.com/2017/09/a-63-year-old-male-recieved-ballon.html
We are talking about this patient: http://bmjcaselogvivek.blogspot.com/2017/09/a-63-year-old-male-recieved-ballon.html
CA 3: I have often seen it being used by many Nephrologists. Is it the result of some providence based pharma trip? Would be good if you can find out more about efficacy of sodium bicarbonate (he had?) in renal failure
CA 4: Is it different from having a tea spoon of baking powder from the kitchen?
CA 3: Perhaps not but would it be advisable in renal failure? We need to look for efficacy of sodium bicarbonate in chronic renal failure
CA 1: Evidence supporting bicarbonate therapy — In addition to the adverse physiologic consequences linked to metabolic acidosis in CKD and the observational studies showing an association of metabolic acidosis with mortality and CKD progression, the rationale behind this approach is based upon randomized trials showing benefits of alkali therapy on:
●Progression of CKD
●Bone health
●Nutritional status
Slowing of CKD progression — Bicarbonate supplementation appears to slow the progression of CKD [77-81]. The best data come from a single-center trial of 134 patients with stage 4 CKD (creatinine clearance, 15 to 30 mL/min/1.73 m2) and metabolic acidosis (baseline serum bicarbonate, 16 to 20 meq/L)randomly assigned to oral sodium bicarbonate, beginning with a dose of 600 mg three times daily and increased as needed to achieve a serum bicarbonate ≥23 meq/L, or to no treatment [77]. At two years of follow-up, the following significant benefits of bicarbonate supplementation were observed:
●A lower mean rate of decline of creatinine clearance compared with the control group (1.88 versus 5.93 mL/min/1.73 m2 per year)
●A lower risk of having an annual decline in creatinine clearance of at least 3 mL/min/1.73 m2(9 versus 45 percent)
●A lower risk of end-stage renal disease (ESRD) (4 versus 22 patients [6.5 versus 33 percent])
Patients in the bicarbonate group were more likely to develop edema and worsened hypertension requiring intensification of therapy, although this difference was not statistically significant. Other concerns about this trial include its open-label design, lack of a placebo control, and small number of events. In addition, the effect size (an 87 percent reduction in the relative risk for ESRD) is considerably larger than the true effects of most rigorously studied interventions
[11:36 AM, 12/25/2017] +880 1752-868045: Two trials by the same investigators demonstrated a benefit from alkali therapy in patients with mild CKD who did not have metabolic acidosis (serum bicarbonate 22 to 24 meq/L). The first trial randomly assigned 120 patients with a mean estimated glomerular filtration rate (eGFR) of 75 mL/min/1.73 m2and an albumin-to-creatinine ratio >300 mg/g to sodium bicarbonate, sodium chloride (each at 0.5 meq/kg per day), or to matching placebo [78]. At five years, the annual rate of decline in eGFR was slightly but significantly smaller in the sodium bicarbonate group (-1.5 min/min/1.73 m2) as compared with the sodium chloride and placebo groups (-2.0 and -2.1 mL/min/1.73 m2, respectively). The second trial randomly assigned 108 patients with stage 3 CKD (eGFR 30 to 59 mL/min/1.73 m2) to usual care or to alkali therapy achieved with sodium bicarbonate supplements or base-producing fruits and vegetables. At three years, eGFR decreased less in the high alkali group [81]. These studies, which enrolled patients with early CKD, suggest that alkali therapy may help to prevent the potentially harmful features associated with the kidney's adaptive response to a decreased number of functioning nephrons and therefore a decreased ability to excrete the daily acid load
●Progression of CKD
●Bone health
●Nutritional status
Slowing of CKD progression — Bicarbonate supplementation appears to slow the progression of CKD [77-81]. The best data come from a single-center trial of 134 patients with stage 4 CKD (creatinine clearance, 15 to 30 mL/min/1.73 m2) and metabolic acidosis (baseline serum bicarbonate, 16 to 20 meq/L)randomly assigned to oral sodium bicarbonate, beginning with a dose of 600 mg three times daily and increased as needed to achieve a serum bicarbonate ≥23 meq/L, or to no treatment [77]. At two years of follow-up, the following significant benefits of bicarbonate supplementation were observed:
●A lower mean rate of decline of creatinine clearance compared with the control group (1.88 versus 5.93 mL/min/1.73 m2 per year)
●A lower risk of having an annual decline in creatinine clearance of at least 3 mL/min/1.73 m2(9 versus 45 percent)
●A lower risk of end-stage renal disease (ESRD) (4 versus 22 patients [6.5 versus 33 percent])
Patients in the bicarbonate group were more likely to develop edema and worsened hypertension requiring intensification of therapy, although this difference was not statistically significant. Other concerns about this trial include its open-label design, lack of a placebo control, and small number of events. In addition, the effect size (an 87 percent reduction in the relative risk for ESRD) is considerably larger than the true effects of most rigorously studied interventions
[11:36 AM, 12/25/2017] +880 1752-868045: Two trials by the same investigators demonstrated a benefit from alkali therapy in patients with mild CKD who did not have metabolic acidosis (serum bicarbonate 22 to 24 meq/L). The first trial randomly assigned 120 patients with a mean estimated glomerular filtration rate (eGFR) of 75 mL/min/1.73 m2and an albumin-to-creatinine ratio >300 mg/g to sodium bicarbonate, sodium chloride (each at 0.5 meq/kg per day), or to matching placebo [78]. At five years, the annual rate of decline in eGFR was slightly but significantly smaller in the sodium bicarbonate group (-1.5 min/min/1.73 m2) as compared with the sodium chloride and placebo groups (-2.0 and -2.1 mL/min/1.73 m2, respectively). The second trial randomly assigned 108 patients with stage 3 CKD (eGFR 30 to 59 mL/min/1.73 m2) to usual care or to alkali therapy achieved with sodium bicarbonate supplements or base-producing fruits and vegetables. At three years, eGFR decreased less in the high alkali group [81]. These studies, which enrolled patients with early CKD, suggest that alkali therapy may help to prevent the potentially harmful features associated with the kidney's adaptive response to a decreased number of functioning nephrons and therefore a decreased ability to excrete the daily acid load
CA 3: Thanks CA 1 went through the information. Not much of patient centered outcomes to merit usage I feel. What do you think?
CA 1: Yes, in the first trial 120 patients with Mild CKD eGFR reduction rate is not so significant?
This is our final short-listed essential drug list:
1. Sacubitril, Valsartan [Cidmus50];
2. Rosuvastatin (10mg), Aspirin low strength (75mg) [Unistar75];
3. Thyrox 25;
4. Stop Glyceryl Trinitrate [Nitrocontin2.6] and continue sorbitrate SOS?;
5. Stop Febuxostat 40
6. Stop Nodosis 500
7. Stop Pancreatin
8. Stop ketosteril and Flavedon MR
9. Continue Metolazone [Zytanix2.5]; and Torsemide [Tide5]
10. Linagliptin (need to asses sugar status and may need to change into other antidiabetics)
This is our final plan and will discuss linagliptin when we will get his blood sugar/HbA1c values.
This is our final short-listed essential drug list:
1. Sacubitril, Valsartan [Cidmus50];
2. Rosuvastatin (10mg), Aspirin low strength (75mg) [Unistar75];
3. Thyrox 25;
4. Stop Glyceryl Trinitrate [Nitrocontin2.6] and continue sorbitrate SOS?;
5. Stop Febuxostat 40
6. Stop Nodosis 500
7. Stop Pancreatin
8. Stop ketosteril and Flavedon MR
9. Continue Metolazone [Zytanix2.5]; and Torsemide [Tide5]
10. Linagliptin (need to asses sugar status and may need to change into other antidiabetics)
This is our final plan and will discuss linagliptin when we will get his blood sugar/HbA1c values.
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