Medicine assessment January 2021
"This is my submission for the Bimonthly internal assessment for the month of January."
Most of the information here have been collected from different reference sites, links to which have been mentioned.The points copy pasted have been put in quotes.The questions to the cases being discussed are from the link below:
https://medicinedepartment.blogspot.com/2021/01/medicine-paper-for-january-2021.html?m=1
Questions:
https://medicinedepartment.blogspot.com/2021/01/medicine-paper-for-january-2021.html?m=1
Questions:
26 year old woman with complaints of altered sensorium somce 1 day,headache since 8 days,fever and vomitings since 4 days
More here: https://harikachindam7.blogspot.com/2020/12/26-year-old-female-with-complaints-of.html
Case presentation links:
https://youtu.be/fz9Jssoc-mA
https://youtu.be/d4lLX04oL8
https://youtu.be/CSCxw2zp7Oc
a). What is the problem representation of this patient and what is the anatomical localization for her current problem based on the clinical findings?
problem:
• headache 1 -2 times /week since 1 month and along with neck pain
• both hands small joint pain and later elbow and shoulder involved. she diagnosis as SLE
• she present to causality with altered sensorium and irrelavent talk
• history of vomittings and generalised weakness ,decreased appetite ,unable to walk
• history of low grade fever and joint pain
More here: https://harikachindam7.blogspot.com/2020/12/26-year-old-female-with-complaints-of.html
Case presentation links:
https://youtu.be/fz9Jssoc-mA
https://youtu.be/d4lLX04oL8
https://youtu.be/CSCxw2zp7Oc
a). What is the problem representation of this patient and what is the anatomical localization for her current problem based on the clinical findings?
problem:
• headache 1 -2 times /week since 1 month and along with neck pain
• both hands small joint pain and later elbow and shoulder involved. she diagnosis as SLE
• she present to causality with altered sensorium and irrelavent talk
• history of vomittings and generalised weakness ,decreased appetite ,unable to walk
• history of low grade fever and joint pain
Anatomical location :
she has low grade fever,chronic headache along with neck pain and altered sensorium.....suggested may be problem in the brain and meninges
1. Hyponatremia secondary to SIADH
2. Tubercular meningitis
3. Acute infarct in the left thalamic region
4. SLE with multiple joint pains
b) What is the etiology of the current problem and how would you as a member of the treating team arrive at a diagnosis? Please chart out the sequence of events timeline between the manifestations of each of her problems and current outcomes.
2. Tubercular meningitis
3. Acute infarct in the left thalamic region
4. SLE with multiple joint pains
b) What is the etiology of the current problem and how would you as a member of the treating team arrive at a diagnosis? Please chart out the sequence of events timeline between the manifestations of each of her problems and current outcomes.
According to the patient history,
the etiology mycobacterium tuberculosis,also the CBNAAT done for csf is positive,indicating Tubercular meningitis
To arrive at a diagnosis,for chronic headache CT or MRI is the preferred modality,
MRI was done and it revealed focal acute infarcts in the left thalamus.
Also lumbar puncture was done it revealed normal protein and cell count but the glucose levels were decreased.
sequence of events
Tubercular meningitis (TBM) is a rare condition in patients with systemic lupus erythematosus (SLE). The aim of this study is to describe the clinical characteristics, possible risk factors, and outcomes of SLE patients with TBM. On systematically reviewing medical records from10 SLE patients with TBM admitted to a hospital from December 2008 to December 2018. A total of 100 cases in the same period were randomly selected as controls from SLE inpatients without infection. In patients with TBM, the mean age at presentation was 35.2 years (range 19.8–45.2); the mean duration of SLE was 34.6 months (range 4–84 months).
Patients with TBM had significantly longer SLE duration, higher ESR and CRP level, and lower CD4+ cell counts and albumin level than those without infections (p < 0.05 for all). There were no differences in prednisone dose at the time of symptom onset or cumulative dose over the preceding year between the two groups. Logistic regression analysis showed that patients with a lower CD4+ cell count were more likely to have TBM compared with controls (OR = 3.67, p = 0.020).
TBM should be considered when SLE patients have central nervous system (CNS) symptoms with a longer duration, higher ESR and CRP level, and lower CD4+ cell counts and albumin level, even if the patients are receiving a low prednisone dose,and the patient being studied has a chronic headache and fits into this criteria
c) What is the efficacy of each of the drugs listed in her prior treatment plan that she was following since last two years before she stopped it two weeks back?
. Hydroxychloroquine
.sulfasalazine
. methylprednisolone
.aceclofenac
. Hydroxychloroquine
.sulfasalazine
. methylprednisolone
.aceclofenac
. cholecalciferol
.alandronic acid
. flupirtine
. gabapentin
. methylcobalamine tablets.
1.Why was she given bisphosphonates?
1) Hydroxychloroquine in SLE
“Chloroquine, together with its hydroxyl derivative hydroxychloroquine, was initially used as an antimalarial agent, but is also useful in the treatment of autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus (SLE).
• Chloroquine and hydroxychloroquine are approved for the treatment of SLE and have been shown to reduce the frequency of disease flares (particularly of lupus nephritis), contribute to the maintenance of remission, prolong the onset of disease and reduce the risk of complications.Beyond their immunomodulatory effects in SLE, these agents have also been shown to protect against thrombotic events, improve glucose and lipid profiles, and prevent renal damage,apparently resulting in reduced cardiovascular risk, for which SLE is an independent risk factor”
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7097534/
2)sulfasalazine
Immunosuppressive drug used in the treatment of cutaneous manifestations of lupus.
“Sulfasalazine is an effective agent for chronic discoid lupus erythematosus (CDLE) but the response to treatment is considerably variable between patients and is also unpredictable. The reason for this might relate to differences in metabolism of the drug which is extensively acetylated by the polymorphic enzyme N-acetyltransferase 2 (NAT2). To test this possibility, the N-acetylation phenotype of eleven patients with CDLE and treated by standard doses of sulfasalazine was retrospectively determined by genotyping. A clear-cut difference in the outcome of treatment was observed according to whether the patients were slow acetylators (SA) or rapid acetylators (RA). Eight out of 11 patients responded to treatment with a complete or marked remission of the disease. Seven of them were RA. The three other patients who did not respond at all to the drug were SA. In addition, SA seem to be more prone to toxic events. These findings strongly suggest that the genetic polymorphism of NAT2 is responsible for differences in the response to sulfasalazine in patients with CDLE. Therefore, candidates for sulfasalazine therapy should be genotyped to identify those patients who might benefit from the drug.”
Source: https://journals.lww.com/jpharmacogenetics/Abstract/1997/04000/NAT2_genotyping_and_efficacy_of_sulfasalazine_in.6.aspx
.alandronic acid
. flupirtine
. gabapentin
. methylcobalamine tablets.
1.Why was she given bisphosphonates?
1) Hydroxychloroquine in SLE
“Chloroquine, together with its hydroxyl derivative hydroxychloroquine, was initially used as an antimalarial agent, but is also useful in the treatment of autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus (SLE).
• Chloroquine and hydroxychloroquine are approved for the treatment of SLE and have been shown to reduce the frequency of disease flares (particularly of lupus nephritis), contribute to the maintenance of remission, prolong the onset of disease and reduce the risk of complications.Beyond their immunomodulatory effects in SLE, these agents have also been shown to protect against thrombotic events, improve glucose and lipid profiles, and prevent renal damage,apparently resulting in reduced cardiovascular risk, for which SLE is an independent risk factor”
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7097534/
2)sulfasalazine
Immunosuppressive drug used in the treatment of cutaneous manifestations of lupus.
“Sulfasalazine is an effective agent for chronic discoid lupus erythematosus (CDLE) but the response to treatment is considerably variable between patients and is also unpredictable. The reason for this might relate to differences in metabolism of the drug which is extensively acetylated by the polymorphic enzyme N-acetyltransferase 2 (NAT2). To test this possibility, the N-acetylation phenotype of eleven patients with CDLE and treated by standard doses of sulfasalazine was retrospectively determined by genotyping. A clear-cut difference in the outcome of treatment was observed according to whether the patients were slow acetylators (SA) or rapid acetylators (RA). Eight out of 11 patients responded to treatment with a complete or marked remission of the disease. Seven of them were RA. The three other patients who did not respond at all to the drug were SA. In addition, SA seem to be more prone to toxic events. These findings strongly suggest that the genetic polymorphism of NAT2 is responsible for differences in the response to sulfasalazine in patients with CDLE. Therefore, candidates for sulfasalazine therapy should be genotyped to identify those patients who might benefit from the drug.”
Source: https://journals.lww.com/jpharmacogenetics/Abstract/1997/04000/NAT2_genotyping_and_efficacy_of_sulfasalazine_in.6.aspx
3.prophylaxis for patients started on corticosteroids?
3)methylprednisolone
Glucocorticoids (GCs) are the mainstay of treatment of SLE as induction therapy and to manage acute flares and have dramatically improved the prognosis of severe SLE.
3)methylprednisolone
Glucocorticoids (GCs) are the mainstay of treatment of SLE as induction therapy and to manage acute flares and have dramatically improved the prognosis of severe SLE.
Intravenous (IV) pulse methylprednisolone therapy, mostly 500-1,000 mg daily for 1-3 days, was introduced in the 1970s (Cathcart, 1976) and is remarkably efficacious in critically ill patients (Isenberg, 1982), suffering renal impairment, central nervous system disease, severe arthritis, pleuropericarditis or thrombopenia.There is still a doubt regarding tapering of the dose of IV methylprednisolone needed to achieve rapid control of activity .
Tapering schedules are mainly based on physician’s experience and clinical judgment.
In patients requiring the therapy adequate prevention of bone loss should be applied, keeping in mind that GC-induced osteoporosis is an early event. Patihents must be immunized against influenza (every year) and Streptococcus pneumoniae (every 5 years)
Source: https://www.eular.org/sysModules/sysFiles/ckeditor_4/plugins/doksoft_uploader/userfiles/18_main_CH21.docx_1.pdf
4)Aceclofenac
“The therapeutic effect of NSAIDs is determined by the suppressed activity of the cyclooxygenase (COX) isoenzymes COX- 1 and COX-2. The widely use of NSAIDs in clinical practice is considerably limited by the risk of adverse reactions (ARs) in the gastrointestinal tract (GIT), which are characteristic for this class of drugs. Medications that are able to selectively inhibit the activity of COX-2 while maintaining that of COX-1 less rarely cause ARs in GIT. This selective effect is produced by aceclofenac. The drug has been also noted to be well tolerated: the risk for aceclofenac- induced ARs in GIT is substantially lower than that due to the use of the majority of other NSAIDs”.
Source:https://mrj.ima-press.net/mrj/article/view/811?locale=en_US
5.cholecalciferol
There is a protective effect of Vitamin D on the immunological abnormalities associated with SLE including its association with downregulation of the T-cell response, proliferation of B-cells, and upregulation of Tregs.
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5361443/
Alandronic acid:
for the prevention and treatment of osteoporosis in Glucocorticoid ‐treated individuals without renal impairment
Source: https://onlinelibrary.wiley.com/doi/full/10.1002/acr.20568
d) Please share any reports around similar patients with SLE and TB meningitis?
• Tubercular meningitis (TBM) is a rare condition in patients with systemic lupus erythematosus (SLE). The aim of this study is to describe the clinical characteristics, possible risk factors, and outcomes of SLE patients with TBM.
• On systematically reviewing medical records from10 SLE patients with TBM admitted to a hospital from December 2008 to December 2018. A total of 100 cases in the same period were randomly selected as controls from SLE inpatients without infection. In patients with TBM, the mean age at presentation was 35.2 years (range 19.8–45.2); the mean duration of SLE was 34.6 months (range 4–84 months). Patients with TBM had significantly longer SLE duration, higher ESR and CRP level, and lower CD4+ cell counts and albumin level than those without infections (p < 0.05 for all). There were no differences in prednisone dose at the time of symptom onset or cumulative dose over the preceding year between the two groups. Logistic regression analysis showed that patients with a lower CD4+ cell count were more likely to have TBM compared with controls (OR = 3.67, p = 0.020).
• TBM should be considered when SLE patients have central nervous system (CNS) symptoms with a longer duration, higher ESR and CRP level, and lower CD4+ cell counts and albumin level, even if the patients are receiving a low prednisone dose,and the patient being studied has a chronic headache and fits into this criteria
Source: https://link.springer.com/article/10.1007/s10067-020-04940-9
Q.Any reports of normal csf leukocyte count and normal csf protein in meningitis?
There is a protective effect of Vitamin D on the immunological abnormalities associated with SLE including its association with downregulation of the T-cell response, proliferation of B-cells, and upregulation of Tregs.
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5361443/
Alandronic acid:
for the prevention and treatment of osteoporosis in Glucocorticoid ‐treated individuals without renal impairment
Source: https://onlinelibrary.wiley.com/doi/full/10.1002/acr.20568
d) Please share any reports around similar patients with SLE and TB meningitis?
• Tubercular meningitis (TBM) is a rare condition in patients with systemic lupus erythematosus (SLE). The aim of this study is to describe the clinical characteristics, possible risk factors, and outcomes of SLE patients with TBM.
• On systematically reviewing medical records from10 SLE patients with TBM admitted to a hospital from December 2008 to December 2018. A total of 100 cases in the same period were randomly selected as controls from SLE inpatients without infection. In patients with TBM, the mean age at presentation was 35.2 years (range 19.8–45.2); the mean duration of SLE was 34.6 months (range 4–84 months). Patients with TBM had significantly longer SLE duration, higher ESR and CRP level, and lower CD4+ cell counts and albumin level than those without infections (p < 0.05 for all). There were no differences in prednisone dose at the time of symptom onset or cumulative dose over the preceding year between the two groups. Logistic regression analysis showed that patients with a lower CD4+ cell count were more likely to have TBM compared with controls (OR = 3.67, p = 0.020).
• TBM should be considered when SLE patients have central nervous system (CNS) symptoms with a longer duration, higher ESR and CRP level, and lower CD4+ cell counts and albumin level, even if the patients are receiving a low prednisone dose,and the patient being studied has a chronic headache and fits into this criteria
Source: https://link.springer.com/article/10.1007/s10067-020-04940-9
Q.Any reports of normal csf leukocyte count and normal csf protein in meningitis?
Q.What could be the probable cause for a normal csf leukocyte count in a patient with chronic meningitis ?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112333/#:~:text=Human%20Parechovirus%20(formerly%20echovirus%2022,when%20suspecting%20aseptic%20viral%20meningitis.
e) What is the sensitivity and specificity of ANA in the diagnosis of SLE?
The estimated sensitivity and specificity of the ANA test for SLE were 100% and 86%, respectively. For other rheumatic diseases, sensitivity and specificity were 42% and 85%, respectively.
https://pubmed.ncbi.nlm.nih.gov/8678710/#:~:text=The%20estimated%20sensitivity%20and%20specificity,11%25%20for%20other%20rheumatic%20diseases.
2) Please go through the two thesis presentations below and answer the questions below by also discussing them with the presenters:
https://youtu.be/sw8o8y5Yw_I
Q.What was the research question in the above thesis presentation?
1)will salt restricted diet decrease blood pressure?
2)can 24hr urinary sodium test reflect the amount of sodium consumed by an individual?
Q.To study the association of serum magnesium levels of type 2 diabetes mellitus
• In this retrospective study 673 diabetic patients were evaluated.
• According to Mg levels, the patients were divided into two groups; as normomagnesemic patients and hypomagnesemic patients.
• There were 55 patients (8.2%) with diabetic retinopathy and 95 patients (14.1%) with diabetic neuropathy. Five hundred patients (74.3%) had normoalbuminuria; 133 patients (19. 8%) had microalbuminuria (MA) and 40 patients (5.9%) had overt proteinuria. One hundred and seventy one patients (25.4%) had HbA1c levels equal or below 7%; and 502 patients (74.6%) had HbA1c levels above 7%. There was no statistical difference in age or duration of diabetes between the groups formed according to Mg levels. Although there were no differences between the groups for retinopathy and neuropathy, MA was more common in hypomagnesemic patients (p =0.004). HbA1c levels did not differ between the groups (p =0.243). However there was a weak negative correlation between serum Mg and HbA1c levels (r =-0.110, p =0.004) and also between serum Mg and urine protein level (r =-0.127, p =0.018
Q.What was the researcher's hypothesis?
• Hypothesis is that, salt restriction doesn't effect blood pressure in all the individuals in the same way, and salt resistant individuals don't benefit from a restricted diet as much as a salt sensitive individual.
Q.What is the current available evidence for magnesium deficiency leading to poorer outcomes in patients with diabetes?
https://youtu.be/jXVS5J1-RNE
Q.What was the research question in the above thesis presentation?
- To study the 24 hour urinary sodium secretion in newly diagnosed hypertensive patient
- Objectives: to analyse the 24 hour urinary sodium with respect to stages of hypertension
- To study effects of sodium on BMI
- analyse 24 hour urinary sodium excretion in complications of hypertension which include opthalmic,renal and cardiovascular changes.
Q.What was the researcher's hypothesis?
- Researcher wanted to find out whether salt restriction in hypertensive patients,as hgave some sort of benefit to them,but in reality there are two categories of patients salt sensitive
- and insensitive groups.It is estimated that 50-60% are salt sensitive and only the sensitive group reacts to changes in dietary salt intake with alterations in blood pressure. It is estimated that about 50-60 % of hypertensives are salt sensitive
- To find out this 24 hour urinary sodium excretion was assessed in Tot
Q.What is the current available evidence for the utility of monitoring salt excretion in the hypertensive population?
The 24hr urinary sodium is a reflection of dietary sodium, and has better results than dietary recall method
https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-10/How-to-quantify-salt-intake-in-certain-patients
Daily salt intake based on 24-hour urinary sodium excretion (assuming that all sodium ingested was in the form of sodium chloride) with a formula: figure 2 shows a practical method to estimate salt or sodium intake.
Figure 2: Calculation for estimation of salt or sodium intake
Na (mg/day) = Na (mmol/day) x 23; NaCl = Na (g/day) x 100/ 39,3
1 gram salt (NaCl) = 393,4 mg Na = 17,1 mmol Na
3) Please critically appraise the full text article linked below:
https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2796.2003.01233.x
What is the efficacy of aspirin in stroke in your assessment of the evidence provided in the article. Please go through the RCT CASP checklist
here https://casp-uk.net/casp-tools-checklists/ and answer the questions mentioned in the checklist in relation to your article.
4) Please mention your individual learning experiences from this month.
1) i learned how to do plural tapping
1)The study answered the research question
being the use of asprin for prevention of stroke progression.
it was foccused in terms of intervention given and outcome measured
2)the method for randomisation was appropriate eliminating systematic bias and allocation sequence concealed from investigators and participants
3)all the participants included in the study were accounted for, including rhe two parcels whixh were accidentally opened.
4)the participants and the investigators were blind methodically
5)the study groups were similar
6)apart from the experimentation, the hospital care given is not documented
7)there were dropouts in the study, study medication was interrupted in few due to suspected side effects,
the p value was not mentioned
8)the cI interval 95%0.6-1.45
9)the treatment effect wasn't much,
10)the outcomes are benefial to my population in prescribing anticoagulants
dual vs single antiplatelet use and longer duration of followup could have been made .
4) Please mention your individual learning experiences from this month.
1) i learned how to do plural tapping
interpretation of ecg
interpretation of LFT report
2)i have seen cases like
.SLE with Tubercular meningitis
.Pancytopenia
.liver abscess with plural effusion
.peripheral vascular disease with supraventricular tachycardia
.pericardial effusion
activities from this month
January 1st, 2nd ,3rd are icu duty
attended rounds at 10 am to 11 am
• Discussed regarding SLE patient with TB meningitis
• Discussed about the drugs causing drugs
January 4th&5th:
Discussed about an elderly woman with AKI on CKD
Attended rounds
presentation about 65 YEAR OLD MALE PATIENT WITH FEVER ,COUGH, SHORTNESS OF BREATH
January 7th:
Attended rounds
1.65 year old man with CKD secondary to diabetes and NSAID use
2.Known case of type 2 DM and hypertension
3.? Anemia of Chronic disease
4. 15 year old boy with Paraparesis since 6 months and a history of fever 6 months back
January 8th:
attended 2 to 4 class
January 9th:
i was in opd
2 cases admission
one is plural effusion with liver abscess
an other on is ansarca ?glomerulonephritis
January 11th:
Attended rounds
Attended 2-4pm class
January 12th
Attended rounds
1)Discussed about a CLD case who is HCV positive and am alcoholic in 2-4pm session
Discussed on Anti HCV drugs
2) i was presented a case about
A 42 YEAR OLD MALE ,FARMER,WITH RIGHT SIDED PLEURAL EFFUSION WITH LIVER ABCESS
January 15th
1)i was presented case in 2 to 4 class about
A 75 year old male with peripheral vascular disease of left lower limb with supraventricular tachycardia
Discussed about a below knee amputation case with Recurrent Atrial Fibrillation
January 16th
i was in opd
admission of 2 cases
one is pericardial effusion
an other one is thrombocytopenia
i have seen the 2d echos of pericardial effusion
i have learned how to remove the pericardial fluid
signs of pericardial effusion
5)
a) What are the possible reasons for the 36 year old man's hypertension and CAD described in the link below since three years?
https://vamsikrishna1996.blogspot.com/2021/01/36-year-male-presented-to-casualty-at.html?m=1
b) Please describe the ECG changes and correlate them with the patient's current diagnosis.
In 1st ecg
irregularly irregular rythmn,normal axis,
Intermittent broad QRS complexes
Remaining ecg
-poor R wave progression with regular rythmn
c) Share an RCT that provides evidence for the efficacy of primary PTCA in acute myocardial infarction over medical management. Describe the efficacy in a PICO format.
https://vamsikrishna1996.blogspot.com/2021/01/36-year-male-presented-to-casualty-at.html?m=1
The possible reasons for hypertension and cad in the given history could be
Alcohol
The HPFS is a prospective investigation of 51 529 US male dentists, pharmacists, veterinarians, optometrists, osteopathic physicians, and podiatrists aged 40 to 75 years who returned a mailed questionnaire about diet and medical history in 1986.
At baseline, men reported their alcohol consumption on a 131-item semiquantitative food frequency questionnaire (FFQ) that included separate items for beer, white wine, red wine, and liquor. Participants were asked how often, on average over the past year, they consumed each beverage. We calculated total alcohol intake by multiplying the average consumption of each beverage by the alcohol content of the specified portion size (12.8 g for beer, 11.0 g for wine, and 14.0 g for liquor) and summing across beverages. The FFQ was administered again every 4 years, with an item for light beer added in 1994. Participants also reported their overall drinking frequency in 1986, 1988, and 1998.
results:
When we compared alcohol intake of 5.0 g/d or more vs less than 5.0 g/d, the hazard ratio was 0.58 (95% CI, 0.37-0.89). Given that 55% of person-time was contributed by consumers of 5 g/d or more of alcohol, we estimate that 25% of the incidence cases of MI in this population were attributable to consuming less than 5 g/d (95% CI, 11%-47%).
Smoking
Temporal Associations Between Smoking and Cardiovascular Disease, 1971 to 2006 (from the Framingham Heart Study)
b) Please describe the ECG changes and correlate them with the patient's current diagnosis.
In 1st ecg
irregularly irregular rythmn,normal axis,
Intermittent broad QRS complexes
Remaining ecg
-poor R wave progression with regular rythmn
c) Share an RCT that provides evidence for the efficacy of primary PTCA in acute myocardial infarction over medical management. Describe the efficacy in a PICO format.
RITA-2 is a randomized control trial published in
Journal of the American College of Cardiology Clinical Trials Vol. 42, No. 7, 2003 © 2003 by the American College of Cardiology Foundation Published by Elsevier Inc.
p-1018,patients recruited at 20 centers in the U.K. and Ireland. In brief, patients with arteriographically proven coronary artery disease (CAD) were considered for the trial if the supervising cardiologist thought that continued medical therapy and PTCA were both acceptable treatment options. Patients had to be over 18 years of age, but there was no upper age limit.
I-The 1,018 patients were randomized to coronary angioplasty (n 504) or continued medical treatment (n 514) from July 1992 to May 1996. Follow-up to September 30, 2001, is included in this report, the median follow-up period being seven years.
C-compared based on death and MI
subsequent interventions required
relief of symptoms of angina and breathlessness
O-Death or myocardial infarction (MI) occurred in 73 (14.5%) PTCA patients and 63 (12.3%) medical patients (difference 2.2%, 95% confidence interval 2.0% to 6.4%, p 0.21). There were 43 deaths in both groups, of which 41% were cardiac-related. Among patients assigned PTCA 12.7% subsequently had coronary artery bypass grafts, and 14.5% required additional non-randomized PTCA. Most of these re-interventions occurred within a year of randomization, and after two years the re-intervention rate was 2.3% per annum. In the medical group, 35.4% required myocardial revascularization: 15.0% in the first year and an annual rate of 3.6% after two years. An initial policy of PTCA was associated with improved anginal symptoms and exercise times. These treatment differences narrowed over time, mainly because of coronary interventions in medical patients with severe symptoms
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