RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES



RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES

BENGALURU, KARNATAKA

PROFORMA FOR REGISTRATION OF SUBJECTS FOR DISSERTATION

|1. |Name of the candidate and address (in block letters) |Dr. MARTIN GEORGE |

| | |DEPARTMENT OF MEDICINE, |

| | |MYSORE MEDICAL COLLEGE AND |

| | |RESEARCH INSTITUTE |

| | |MYSORE-570001 |

|2. |Name of the Institution |MYSORE MEDICAL COLLEGE AND |

| | |RESEARCH INSTITUTE |

| | |MYSORE-570001 |

| | |POSTGRADUATE IN GENERAL MEDICINE |

|3. |Course of the study and subject | |

|4. |Date of admission to course |19/08/2013 |

|5. |Title of the topic |

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| |“ASSESSMENT OF LEFT VENTRICULAR SYSTOLIC FUNCTION IN SUBJECTS ADMITTED WITH ISCHEMIC STROKE IN MEDICAL INTENSIVE CARE |

| |UNIT OF A TERTIARY CARE HOSPITAL ” |

|6. |Brief resume of the intended work |

|6.1 |Need for the study |

| |Symptomatic heart failure is present in 0.4% to 2% of the population 1and continues to rise as the population ages(1) In |

| |order to substantially reduce and/or delay the incidence of heart failure and its consequences, we need to detect and treat |

| |pre symptomatic left ventricular (LV) dysfunction which is the main cause of heart failure. |

| |It is clear that angiotensin-converting enzyme (ACE) inhibitors and beta-blockers can prevent the progression of LVSD to |

| |heart failure and reduce morbidity and mortality. In addition, spironolactone, warfarin and implantable |

| |cardioverter-defibrillators (ICDs) are possible therapies in selected cases. Indeed, ICD placement is a new therapy that |

| |particularly benefits those with LVSD (2-4). |

| |Left ventricular systolic dysfunction is found in 2% to 12% of the general population, with >60% of subjects being |

| |asymptomatic. But such cases are detected only at very late stage, where the treatment is less effective. So an effective |

| |screening method which can detect asymptomatic LVSD will help in providing early treatment which will significantly reduce |

| |the morbidity and mortality. [5-6] |

| |Many screening studies have focused on the general population, but screening whole populations is unlikely to be |

| |cost-effective. More selective screening for LVSD is already routinely undertaken in post-myocardial infarction (MI) |

| |subjects while they are in the coronary care unit. Subjects who present with their first non cardiac episode such as |

| |ischemic stroke represent another high-risk group that might be worth screening for treatable LVSD.(7) |

| |Studies shown the relationship between LVSD and ischemic stroke. But, it is ironic that after an ischemic stroke, it is |

| |standard practice to optimize the treatment of distant risk factors, such as blood pressure and cholesterol, and yet we |

| |ignore whether a bigger risk factor, like LVSD, already exists. This is even stranger when one considers that LVSD is easily|

| |detected by a noninvasive test and easily treated by beta-blockers, ACE inhibitors, spironolactone, warfarin, ICDs or a |

| |combination of these [13] . |

| |A significant amount of cardiac deaths can be preventable by identifying and agressively treating LVSD at the earliest. |

| |Thus the reason for wanting to know the extent of LVSD in ischemic stroke is that such cases might have a greater |

| |incidence of LVSD, and it may be very cost-effective to screen for treatable LVSD in such cases. |

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| |Review of literature |

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|6.2 | |

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| |The most frequently recognized reasons for cardioembolic stroke in subjects with CHF are thrombus formation due to AF or |

| |left ventricular (LV) hypokinesia.[8] |

| |1. LV dysfunction causes an increased LV end diastolic volume that promotes the blood stasis in both LV and |

| |left atrium,increasing the chance of thrombus formation and the risk of embolic stroke.[9] |

| |2. As a consequence of the activation of the sympathetic nervous system and of the renin-angiotensin-aldosterone system, |

| |there is a hypercoagulable state, increased aggregation of thrombocytes, and reduced fibrinolysis in subjects with CHF. |

| |Moreover, there is evidence of endothelial dysfunction in CHF subjects, rheological alterations consistent with increased |

| |blood velocity, and malfunctioning of cerebral autoregulation. (9) |

| |3.Cerebral hypoperfusion that is caused by the hypotension in LVSD is an additional risk factor for stroke .But in subjects |

| |with adequate ceribrovascular reactivity this hypotension is compensated by lowering cerebrovascular resistance through |

| |dilatation of the brain arterioles. This is called autoregulation. [11] However, subjects with HF may easily decompensate |

| |hemodynamically and may become hypotensive secondary to cardiac ischemia, arrhythmia or over-medication with hypotensive |

| |drugs. This would limit the potential for further dilatation, resulting in the altered cerebrovascular reserve capacity |

| |observed in subjects with HF. Increasing severity of HF, indicated by NYHA grade and decreasing EF, are correlated with |

| |decreased cerebrovascular reactivity and decreased global cerebral blood flow(12) |

| |In addition to the causal relation between LVSD and ischemic stroke, both entities represent manifestations of similar |

| |underlying risk factors, such as hypertension and diabetes mellitus ,smoking.(10) |

| |1.Survival and Ventricular Enlargement (SAVE) (14) was a prospective trial with 5 years follow-up that assessed the relation|

| |between LVEF and the incidence of stroke in2231 subjects who have asymptomatic LVSD. LVEF was found to be an independent |

| |risk factor. For every 5% decrease in EF there was an 18% increase in the risk of stroke. In addition, subjects with EF |

| |lower than 28% had a relative risk of stroke of 1.86, compared with subjects with higher LVEF. |

| |2. Low EF was a risk factor for stroke in the multiethnic North Manhattan (NOMASS) population cohort, |

| |independently of age, sex and ethnicity; however, risk of stroke was not related to severity of EF reduction .(15) |

| |3.The TOAST (Trial of Org 10172 in Acute Stroke Treatment) (16)classification , the most widely accepted etiological |

| |classification of ischemic strokes, included symptomatic HF with low EF and chronic myocardial infarction (MI) with EF less|

| |than 28% as primary high risk sources of embolic stroke. |

| |4.The study cohort included 630 persons with incident HF(17). During a median of 4.3 years of follow-up, 102 (16%) |

| |experienced an ischemic stroke. Heart failure was associated with a 17.4-fold increased risk for stroke compared with the |

| |general population in the first 30 days after HF diagnosis and remained elevated during 5 years of follow-up. |

| |5. In the Reasons for Geographic And Racial Differences in Stroke (REGARDS) (18), a U.S. population study that has included|

| |more than 30 000 participants. The adjusted OR for the association between HF and stroke/TIA was 3.0 (95% CI: 2.2-4.0) . |

| |6.Interestingly, a retrospective analysis of the Studies of Left Ventricular Dysfunction (SOLVD) (18) study also |

| |demonstrated relevant sex differences for CHF subjects without AF. SOLVD data found a 58% increase in risk of |

| |thromboembolic events for every 10% decrease in EF among women.But no assossiation in case of males. |

| |7.The recent Heart Outcomes Prevention Evaluation(HOPE) (20) study shown that treating all high risk subjects with ramipril|

| |will reduce cardiac events.It emphasis the need for early diagnosis of LV dysfunction like important risk factors. |

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| |Objectives of the study |

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| |1.To study the prevalence of left ventricular (LV) systolic dysfunction (LVSD) in subjects who present with ischemic |

| |stroke. |

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| |2.To study the relation of ischemic stroke with severity of reduction of ejection fraction. |

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|6.3 | |

|7. |Material and Methods |

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| |A. Source of data |

|7.1 |50 Subjects admitted in medical intensive care of K.R.Hospital Mysore and who satisfy the inclusion criteria will be studied during a |

| |period from January 2014 to January 2015. |

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| |Method of collection of data : |

| |A 50 Subjects including both male and female who admitted in medical intensive care is selected by purposive sampling. Informed |

| |written consent shall be taken from all the subjects. A pre structured performa will be used to collect the baseline data. Detailed |

| |clinical examination and required investigations will be done on all subjects. |

|7.2 |LVSD is assessed by Two-dimensional echocardiography . |

| |Left ventricular systolic dysfunction was defined as an ejection fraction ≤40%.(This value is made as cutoff, because it represents the|

| |value used in many ACE inhibitor studies of subjects with LV dysfunction, and this is the level of function below which ACE inhibitor |

| |therapy is commonly prescribed. ) [20] |

| |Symptomatic LV dysfunction was defined by the presence of symptoms of cardiac dyspnoea, fatigue, orthopnoea and paroxysmal nocturnal |

| |dyspnoea. |

| |Asymptomatic LV dysfunction was defined by the absence of such cardiac symptoms. |

| |Blood pressure was recorded with sphygmomanometer, supine position after a 5-min rest. |

| |Standard 12-lead electrocardiograms (ECGs) were recorded and classified for the presence of atrial fibrillation, atrial flutter, left |

| |bundle branch block, LV hypertrophy, pathologic Q waves and ischemia. Ischemia included ST-segment depression, any T-wave inversion and |

| |Q waves |

| |The clinical definitions that used in this study are as follows. Ischemic heart disease (IHD) was defined as a history of chronic |

| |stable angina/unstable angina, MI or taking anti-anginal medications. |

| |Hypertension included a known history of such or a history of taking antihypertensive medications, or both, or blood-pressure values |

| |>140/90 mm Hg during the hospital stay. |

| |Hypercholesterolemia referred to a subject with known total serum cholesterol >200mg/dl or a subject on a cholesterol-lowering diet, |

| |medication or both. |

| |Smoking referred to subjects with a history of cigarette smoking at the time of the ischemic stroke or to current smokers. |

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| |B. Inclusion Criteria |

| |Subjects with stroke, diagnosed by the clinical examination and confirmed as ischemic by the CT scan or MRI brain. |

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| |C. Exclusion Criteria: |

| |1.subjects with previous history of stroke . |

| |2.previous proven heart failure cases. |

| |3.subjects already on cardiac failure medications. |

| |4.known cases of congenital heart diseases. |

| |5.known cases of rheumatic heart diseases. |

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| |D. Method of study |

| |Study design |

| |Explorative study |

| |Total study time -18 months |

| |January 2014 to july 2015 |

| |Data collection time-1 year |

| |January 2014 to January 2015 |

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| |E. Statistical analysis |

| |Statistical methods used are descriptive statistics, chi-square tests, contigency coefficient analysis. |

| |A probability value ................
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