Left Ventricular Hypertrophy in Young Africans With First Ever Stroke in Tanzania: A Prospective Cohort Study 

DOI: https://doi.org/10.21203/rs.3.rs-324415/v1

Abstract

Background: Left ventricular hypertrophy is a pathophysiological response to chronic hypertension and is an independent risk factor for vascular events. We sought to determine the magnitude, correlates and prognosis of left ventricular hypertrophy in young patients presenting with their first stroke at a tertiary hospital. We also sought to determine the accuracy of electrocardiography using Sokolow-Lyon and Cornell criteria in detecting left ventricular hypertrophy compared to echocardiography.

Methods: This cohort study prospectively recruited consecutive stroke patients aged 18-45 years who had undergone brain imaging, electrocardiogram and transthoracic echocardiography. Baseline data were recorded and correlates of left ventricular hypertrophy were identified using the modified Poisson regression. Follow-up for functional outcomes was performed to 30-days using the modified Rankin Scale.

Results: We enrolled 101 participants with first ever stroke. The mean age of patients was 39.7years and the mean National Institutes of Health Stroke Score was 18, reflecting severe disability. Brain imaging revealed ischemic strokes in 60 (59.4%) of patients and of those with intracerebral hemorrhage, 33 (86.8%) were localized to the basal ganglia, in keeping with a hypertensive etiology. Left ventricular hypertrophy was present in 76 (75.3%; 95% CI 65.7% – 83.3%), and 30 (39.5%) and 28 (36.8%) had moderate to severe degree respectively. Young adults with left ventricular hypertrophy were more likely to have a higher systolic and diastolic blood pressure on arrival 156.3±19 and 96.4±10.6 respectively. On multivariable analysis, lack of antihypertensive medication was associated with left ventricular hypertrophy {adjusted risk ratio 1.42 (95% CI: 1.04–1.94). The sensitivity and specificity for Sokolow-Lyon in detecting left ventricular hypertrophy was 27% and 78%, and for Cornell was 32% and 52% respectively. At 30-days, functional independence was achieved in 12 (12.4%) and almost half had died.

Conclusions: There is a high burden of left ventricular hypertrophy in young patients with first stroke. Untreated hypertension is the likely etiology associated with a high 30-day mortality. Our findings did not support the use of the electrical voltage criteria for detecting left ventricular hypertrophy. We recommend low cost interventions such as blood pressure screening and control to reduce this burden in the young.

Background

Stroke is the leading cause of death and disability in low and middle income countries (LMICs) accounting for 80% of the global burden (1). Cardiovascular diseases, particularly hypertension, is the leading risk factor for stroke in both high and LMICs and is responsible for 20-50% of all strokes (2–4). In sub Saharan Africa (SSA) including Tanzania, 50% of stroke among the young population is attributed to uncontrolled hypertension (5) and 45% of all stroke cases could be prevented by adequate blood pressure control (6,7).

Left ventricular hypertrophy (LVH) is a common complication of long standing uncontrolled arterial hypertension, occurring as a pathophysiological adaption to chronic increased afterload (8). This abnormal increase in the left ventricular mass serves as an independent predictor for coronary events, heart failure, ventricular arrhythmias, stroke and peripheral arterial disease (9). Previous reports have indicated an increased incidence of stroke among elderly with LVH and is included in the original 10-year Framingham stroke risk score for prediction of stroke in the geriatric population (10). In SSA, there is a high burden of LVH (up to 50%) particularly among untreated hypertensive patients (11). A study in West Africa revealed that more than half of the stroke patients were found to have LVH by electrocardiogram. Independent predictors for LVH were: younger age (<45 years), female gender and uncontrolled hypertension (12).

Transthoracic echocardiography (TTE) is a noninvasive modality of choice to assess cardiac structure and function (including the detection of LVH) (13). It is considered gold standard and superior to the 12-lead electrocardiogram (ECG) for diagnosing LVH (14). In Tanzania, little is known about the burden and outcomes of LVH among young adults with stroke. We aimed to investigate the magnitude, correlates and outcomes of LVH among young adults with stroke admitted at a tertiary hospital in Tanzania. We also sought to determine the accuracy of electrocardiography using Sokolow-Lyon and Cornell criteria in detecting LVH compared to echocardiography.

Methods

Study design and population:

This prospective cohort study was conducted at Muhimbili University of Health and Allied Sciences Academic Medical Center (MAMC), medical wards in Dar es Salaam, Tanzania. MAMC is a tertiary teaching hospital that offers super specialized medical care to all specialties and receives referral patients from both public and private hospitals from all over the country.

We recruited consecutive participants who were admitted at MAMC with a clinical diagnosis of first ever stroke as classified by the World Health Organization (WHO) (15) between June 2018 to January 2019. Participants were eligible for enrollment if they were aged between 18 to 45 years. Written informed consent was obtained from either the participants or their next of kin if the participant was unable to consent prior to study enrollment.

Data collection:

An interviewer based structured questionnaire was administered to all study participants or their caregivers capturing the following: sociodemographic information, mobile numbers, premorbid stroke risk factors (e.g. hypertension, diabetes mellitus (DM), smoking, alcohol consumption and HIV infection). Medication history for hypertension, diabetes and HIV was also obtained.

Physical examination included measurement of blood pressure (BP) using a standard digital BP machine, AD Medical Inc. Three BP readings were collected spaced 5 minutes apart, while the participant was at rest and an average BP was computed. Hypertension was defined as a systolic blood pressure (SBP) ≥140 mmHg or diastolic blood pressure (DBP) ≥90 mmHg or those on current anti-hypertensive therapy according to the Joint National Committee 7 (JNC-7) definition (16). All participants had their waist and hip circumference measured using a tape measure and recorded in centimeters. The waist-hip ratio was interpreted according to the WHO guidelines; in males the ratio of ≥0.90 and females ≥0.85 was regarded as substantially increased (17).

Capillary fingertip blood samples were collected to check for random blood glucose (RBG) levels and HIV rapid testing using a glucometer GLUCOPLUSTM and SD Bioline respectively. A fasting blood glucose (FBG) sample was collected the following morning for participants with (RBG) levels of ≥11.1 mmol/l. DM diagnosis was defined as a RBG reading of ≥ 11.1 mmol/l or a FBG reading of ≥ 7 mmol/l. For participants who were HIV reactive to SD Bioline, were tested also using Unigold Biotech.

We aseptically collected 5mls of venous blood from each study participant and analyzed for random total cholesterol and low-density lipoprotein using BIO- SYSTEMS machine.

A non-contrast brain computed tomography scan (NCCT) using GE Healthcare Optima or magnetic resonance imaging (MRI) with GE SIGNA CREATOR were performed on study participants on admission and images interpreted by a senior radiologist.

TTE using GE Medical Systems was performed and interpreted by a qualified cardiologist. Evidence of LVH was defined according to the European Society of Cardiology/American Society of Echocardiography as a measure of severity of septal thickness in 4 chamber view at mid-septum in the end of diastole (18). A mid septal diameter of 11 – 13mm in males and 10 – 12 mm in females was defined as mild LVH, 14 – 16 mm in males and 13 – 15 mm in females as moderate LVH and ≥17 mm in males and ≥16 mm in females as severe LVH (19).

An ECG using Bionet model Cardio7 machine was performed on the study participants to look for evidence of LVH using the Sokolow-Lyon and Cornell criteria defined as S in V1 plus R in V5 or V6 required to surpass 3.5 mV (20), and the S in V3 plus R in aVL required to surpass 2.0 mV in females and 2.8 mV in males (21) respectively. Atrial fibrillation was defined as the presence of irregular RR intervals and no discernible distinct P waves (22).

Stroke severity was assessed using the  National institute of health stroke scale (NIHSS) (15) and outcomes were assessed using the modified Rankin Scale (mRS) (15) at 24 hours, 72 hours, 7 days, 14 days and at 30 days from admission. Functional independence was defined as mRS score of 0-2.

Data analysis:

Data was analyzed using SPSS version 20.0. Continuous variables were summarized and presented as means and standard deviation (SD). Categorical variables were summarized as frequencies and proportions. Comparison between proportions were done using Pearson’s Chi square test or Fisher’s exact test. The outcome variable (LVH) was common, hence we used the modified Poisson regression to determine factors that were independently associated with LVH. All covariates with a p-value of <0.2 in bivariable analysis were included in the multivariable analysis model. Unadjusted and adjusted risk ratios (RR), 95% confidence intervals (CI) and corresponding p values were obtained from the models. A two-tailed significance level was set as a p value of < 0.05. Receiver operator characteristics (ROC) analysis was performed to estimate the performance of the electrical voltage criterions (Sokolow-Lyon and Cornell criterion) to the gold standard TTE in detecting LVH.

Results

There were a total of 484 medical admissions of patients aged ≤45 years between June 2018 to January 2019, of whom 128 (26.4%) participants met the World Health Organization (WHO) clinical diagnosis of first ever stroke (15). We excluded 27 (21.1%) participants for the following reasons: unable to consent 5 (3.9%), did not complete brain imaging 6 (4.7%) and did not undergo TTE 16 (12.5%). The remaining 101 young adults with stroke were recruited. There were 4 participants who were lost to follow-up and were excluded from the outcome analysis, Figure 1.

The proportion of LVH confirmed by TTE among the young stroke participants was 76 (75.3%; 95% CI 65.7% – 83.3%). The mean age±SD of the recruited participants was 39.7±2 years, whereas the mean NIHSS was 18.3±9.2, reflecting severe disability. Less than a third of the study participants had health insurance 29 (28.7%). The majority of the young stroke participants had a previous history of hypertension 66 (65.3%). The overall mean systolic and diastolic blood pressures at enrollment were 153.5±20.1 mmHg and 94.5±11.4 mmHg (Table 1). However, the young stroke participants with LVH were more likely than without LVH to have a higher systolic and diastolic blood pressure, 156.3 ± 19 vs 145.1 ± 19.5 mmHg, p=0.017 for systolic blood pressure (SBP) and 96.4 ± 10.6 vs 89 ± 12.2 mmHg, p=0.01 for diastolic blood pressure (DBP) respectively. The majority of young stroke participants had moderate 30 (39.5%) to severe 28 (36.8%) LVH as summarized in figure 2.

Table 2 summarizes the stroke subtype among the young stroke participants with LVH and without LVH. Ischemic stroke was the major stroke subtype accounting for 60 (59.4%) of all young strokes. There was no statistical significant difference in stroke subtype among the two groups. The location of the hemorrhages was intracerebral in 38 (92.7%) and subarachnoid in 3 (7.3%). Among those with intracerebral hemorrhage, 33 (86.8%) were in the basal ganglia.

Factors associated with LVH are summarized in Table 3. In bivariable analysis, factors that were significantly associated with LVH among the young stroke participants were: hypertension, not on anti-hypertensive medication, family history of hypertension and hypercholesteremia. In multivariable analysis after adjusting for other factors, lack of anti-hypertensive medication was the only independent factor for LVH {adjusted RR 1.42 (95% CI: 1.04–1.94)}.

Mortality at 30 days was 42 (43.3%), with no statistically significant difference in mortality between young strokes with and without LVH. A total of 55 (56.7%) participants survived to 30-days, those who achieved functional independency (mRS 0-2) were 8 (11%) and 4 (16.7%) among young strokes with LVH and without LVH respectively (Table 4).

The sensitivity and specificity analysis for the detection of LVH using the electrical voltage criteria (Sokolow-Lyon and Cornell criteria) are presented in Table 5. ECG could not be performed on 10 young stroke participants and were excluded from this analysis. The sensitivity and specificity for the Sokolow-Lyon criteria in detecting LVH was 27% and 78% and for Cornell criteria was 32% and 52% respectively. The ROC analysis was also carried out and the results are shown in Figure 3. Both criterions did not reach statistical significance, for Sokolow-Lyon criteria area under the curve (AUC)= (0.55 [95% CI 0.42 – 0.69], p=0.44) and Cornell criteria AUC= (0.48 [95% CI 0.33 – 0.63], p=0.78).

Discussion

This study aimed to investigate the burden and early outcomes of LVH among young adults with first ever stroke admitted at a tertiary hospital in Tanzania. We found that three-quarters of young stroke participants had LVH as diagnosed by TTE, which is higher than that described in a West African study by Adeoye et al, were 55% of the blacks (mean age of 59.1±13.2 years) with first stroke had LVH (12). The authors also found that younger age ≤45 years was independently associated with LVH, suggesting an underlying genetic factor in the pathogenesis which merits further investigation. Our findings also reveal a higher proportion of LVH compared to studies in high income countries in comparable populations. For instance, in the United States, Luciana et al found 30% of young adults with first stroke had LVH on TTE (23) and Levy et al describes a prevalence of 6% among adults under 30 years (24). This difference in proportions could be explained by the different ethnicity; ours exclusively an African population. Numerous reports have indicated that ethnicity plays an important role in the epidemiology of LVH (13,25,26); Compared to whites, Africans with or without stroke are more likely to have LVH across all age groups.

LVH is the increase in ventricular mass either due to an increase in wall thickness, in cavity size, or both (9). Hypertension plays a crucial role in the pathogenesis of LVH, which in turn is an independent risk factor for end organ damage (27). In this study, young stroke participants with LVH were statistically more likely to have uncontrolled hypertension supported by the fact that they had a higher mean systolic and diastolic blood pressures on hospital arrival compared to those without LVH. Similarly, more than a third of the young stroke participants with LVH had deep basal ganglia intracerebral hemorrhage on brain imaging, in keeping with the known pathophysiology of this stroke subtype. Hypertensive hemorrhages typically occur in these regions as the penetrating arteries are susceptible to rupture due to hypertension (28).

Remarkably, the majority of our young stroke participants had moderate to severe degree of LVH by TTE. This implies that the elevated blood pressure readings observed in our study population were less likely a result of the auto-regulatory mechanisms commonly seen in acute stroke, but rather a chronic adaptation to long standing undiagnosed hypertension. Longitudinal studies have established that cardiac end organ damage progresses from young adulthood to middle age and is compounded by hypertension, DM and tobacco smoking (29). Similarly, several studies have demonstrated an increased risk of stroke among individuals with LVH secondary to hypertension (30,31). This merits the need for early screening to detect hypertension during the adolescent period at secondary schools, long before end organ damage manifests. Further research is needed on the etiology of hypertension in young African adults.

It is notable that not taking anti-hypertensive medications was the only independent factor associated with LVH among the young stroke participants, in line with other studies (32). In this study, the majority of young participants had premorbid hypertension. Non-adherence or undertreated hypertension are likely causes of this uncontrolled hypertension and warrants further research. Possible causes of non-adherence to treatment could be lack of insurance, which was seen in less than a third of the study participants. The need for treatment and control of hypertension cannot be overemphasized in SSA (4,33). This calls for urgent community awareness and campaigns promoting the importance of drug adherence in chronic illnesses.

In this study, we observed a high 30-day mortality, seen predominantly in patients with LVH. This suggests that primary prevention is the main route to reducing the burden from LVH and stroke, as once young adults succumb to stroke, their prognosis is generally poor and leads to a decline in the family and nation’s economy.

Given the cost and availability of TTE, we also aimed to assess the performance of the electrical voltage criteria for detecting LVH compared to TTE. We found that both the Sokolow-Lyon and Cornell criteria had a low sensitivity, moderate specificity and poor performance in detecting LVH in our population, making it a less accurate and unreliable method. Therefore, the key public health message from this research is that efforts should be centered at promoting low cost interventions such as blood pressure screening, treatment and control which could reduce the burden of LVH and stroke in young Africans.

Our study had the following limitations; it was a single center with a small sample size therefore there was limited power to detect the differences between the two groups and the results cannot be generalized.

Conclusions

We identified a high proportion of young strokes with LVH. Untreated hypertension was the likely etiology and was associated with a high 30-day mortality. Further studies are recommended to investigate the etiologies of hypertension and causes of non-adherence or under treatment with medications. This will help identify sustainable interventions that will support prevention, detection and treatment of hypertension in young adults to reduce the burden of stroke.

List Of Abbreviations

AF: Atrial Fibrillation

DALYS: Disability Adjusted Life Years

DWI: Diffusion Weighted Image

FBG: Fasting Blood Glucose

HIV: Human Deficiency Virus

mRS: Modified Rankin Scale

NIHSS: National Institute of Health Stroke Scale

SSA: sub Saharan Africa

TTE: Trans thoracic echocardiography

WHO: World Health Organization

Declarations

Ethical approval and consent to participate: Ethical clearance was obtained from Muhimbili University of Health and Allied Sciences Institutional review board approval number DA.287/298/01A/. The study was carried out in accordance with the tenets of the Declaration of Helsinki. Written informed consent to take part in the study and for HIV testing was obtained from all study participants or their next of kin prior to study enrollment. All patients were offered standard of care following diagnosis.

Consent for publication: Not applicable.

Availability of data and materials: Data are available from the corresponding author on reasonable request.

Competing interests: We declare no competing interests.

Funding: This study was funded by Catholic University of Health and Allied Sciences. The funder had no role in the design, analysis, final write up of the manuscript and decision to submit the paper for publication.

Authors contributions: SSM, PM and KM conceptualized and designed the study. SSM and KK collected data. SSM, CM and PM performed data analysis and interpreted the results. SSM, KM, KK and CM drafted the initial manuscript. All authors critically reviewed and revised the final manuscript.

Acknowledgement: Our sincere gratitude goes to the study participants for taking part in this study.

References

  1. Krishnamurthi R V., Ikeda T, Feigin VL. Global, Regional and Country-Specific Burden of Ischaemic Stroke, Intracerebral Haemorrhage and Subarachnoid Haemorrhage: A Systematic Analysis of the Global Burden of Disease Study 2017. Neuroepidemiology. 2020;54(2):171–9.
  2. O’Donnell MJ, Chin SL, Rangarajan S, Xavier D, Liu L, Zhang H, et al. Global and regional effects of potentially modifiable risk factors associated with acute stroke in 32 countries (INTERSTROKE): a case-control study. Lancet. 2016;388(10046):761–75.
  3. Willey JZ, Moon YP, Kahn E, Rodriguez CJ, Rundek T, Cheung K, et al. Population attributable risks of hypertension and diabetes for cardiovascular disease and stroke in the Northern Manhattan study. J Am Heart Assoc. 2014;3(5).
  4. Walker RW, Jusabani A, Aris E, Gray WK, Unwin N, Swai M, et al. Stroke risk factors in an incident population in urban and rural Tanzania: A prospective, community-based, case-control study. Lancet Glob Heal. 2013;1(5):282–8.
  5. Matuja, SS, P M, K K. The burden and outcomes of stroke in young adults at a tertiary hospital in Tanzania : a comparison with older adults. BMC Neurol. 2020;20(1):206.
  6. Obiako O, Ogunniyi A, Oparah S. Prognosis and outcome of acute stroke in the University College Hospital Ibadan, Nigeria. Niger J Clin Pract. 2011;14(3):359.
  7. Deresse B, Shaweno D. Epidemiology and in-hospital outcome of stroke in South Ethiopia. J Neurol Sci. 2015;355(1–2).
  8. Marwick TH, Gillebert TC, Aurigemma G, Chirinos J, Derumeaux G, Galderisi M, et al. Recommendations on the Use of Echocardiography in Adult Hypertension: A Report from the European Association of Cardiovascular Imaging (EACVI) and the American Society of Echocardiography (ASE). J Am Soc Echocardiogr. 2015 Jul 1;28(7):727–54.
  9. Desai CS, Bartz TM, Gottdiener JS, Lloyd-Jones DM, Gardin JM. Usefulness of Left Ventricular Mass and Geometry for Determining 10-Year Prediction of Cardiovascular Disease in Adults Aged >65 Years (from the Cardiovascular Health Study). Am J Cardiol. 2016;118(5):684–90.
  10. Wolf PA, D’Agostino RB, Belanger AJ, Kannel WB. Probability of stroke: A risk profile from the framingham study. Stroke. 1991;22(3):312–8.
  11. Chillo P, Lwakatare J, Rieck ÅE, Lutale J, Gerdts E. Prevalence and covariates of abnormal left ventricular geometry in never-treated hypertensive patients in Tanzania. Blood Press. 2014;23(1):31–8.
  12. Adeoye AM, Ovbiagele B, Kolo P, Appiah L, Aje A, Adebayo O, et al. Exploring Overlaps Between the Genomic and Environmental Determinants of LVH and Stroke: A Multicenter Study in West Africa. Glob Heart. 2017;12(2):107-113.e5.
  13. Drazner MH, Dries DL, Peshock RM, Cooper RS, Klassen C, Kazi F, et al. Left ventricular hypertrophy is more prevalent in blacks than whites in the general population: The Dallas heart study. Hypertension. 2005 Jul;46(1):124–9.
  14. Quispe-Tintaya W. HHS Public Access. Physiol Behav. 2017;176(3):139–48.
  15. WHO Noncommunicable Diseases and Mental Health. The WHO STEPwise approach to stroke surveillance report [Internet]. 2005. Available from: https://www.who.int/ncd_surveillance/en/steps_stroke_manual_v1.2.pdf
  16. Chobanian A V., Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Vol. 42, Hypertension. Lippincott Williams & Wilkins; 2003. p. 1206–52.
  17. World Health Organization. Waist Circumference and Waist-Hip Ratio: Report of a WHO Expert Consultation. Who. 2011;(8-11 December 2008):1–39.
  18. Lang R, Bierig M, Devereux R, Flachskampf F, Foster E, Pellikka P, et al. Recommendations for chamber quantification☆. Eur J Echocardiogr. 2006 Mar 1;7(2):79–108.
  19. Lang RM, Badano LP, Victor MA, Afilalo J, Armstrong A, Ernande L, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: An update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28(1):1-39.e14.
  20. Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J. 1949 Feb 1;37(2):161–86.
  21. Casale P, Devereux R, Kligfield P, Eisenberg R, Miller D, Chaudhary B, et al. Electrocardiographic detection of left ventricular hypertrophy: development and prospective validation of improved criteria. JAA. 1985;6(3):573–80.
  22. Benussi S. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Eur Heart J. 2016;37(38):2893–962.
  23. Catanese L, Shoamanesh A, Lau H, Romero J, Babikian V, Kase C, et al. Left Ventricular Hypertrophy as a Predictor of White Matter Hyperintensities in Young Stroke Patients (P2.111). Neurology. 2014;82(10 Supplement):111.
  24. Levy D, Anderson KM, Savage DD, Kannel WB, Christiansen JC, Castelli WP. Echocardiographically detected left ventricular hypertrophy: Prevalence and risk factors. The Framingham heart study. Ann Intern Med. 1988;108(1):7–13.
  25. Yan Hou, Elizabeth Aradine, Kathleen Ryan, Prachi Mehndiratta, Seemant Chaturvedi, Carolyn A Cronin, Michael S Phipps, Marcella A Wozniak, Jose G Merino-Juarez, Tara M Dutta, John W Cole SJK. African American Young Adults with Ischemic Stroke Have High Rates of Left Ventricular Hypertrophy | Stroke [Internet]. American Stroke Association. 2020 [cited 2020 Dec 11]. p. 200. Available from: https://www.ahajournals.org/doi/10.1161/str.51.suppl_1.TP200
  26. Kamath S, Markham D, Drazner MH. Increased prevalence of concentric left ventricular hypertrophy in African-Americans: Will an epidemic of heart failure follow? Heart Fail Rev. 2006;11(4):271–7.
  27. Katholi RE, Couri DM. Left ventricular hypertrophy: Major risk factor in patients with hypertension: Update and practical clinical applications. Vol. 2011, International Journal of Hypertension. 2011.
  28. JH G, Ho K. Pathology of hypertensive arteriopathy - PubMed. Neurosurg Clin N Am. 1992;3(3):497–501.
  29. Gidding SS, Liu K, Colangelo LA, Cook NL, Goff DC, Glasser SP, et al. Longitudinal determinants of left ventricular mass and geometry: The coronary artery risk development in young adults (CARDIA) study. Circ Cardiovasc Imaging. 2013;6(5):769–75.
  30. Verdecchia P, Angeli F, Gattobigio R, Sardone M, Pede S, Reboldi GP. Regression of Left Ventricular Hypertrophy and Prevention of Stroke in Hypertensive Subjects. Am J Hypertens. 2006;19(5):493–9.
  31. Bots ML, Nikitin Y, Salonen JT, Elwood PC, Malyutina S, Freire de Concalves A, et al. Left ventricular hypertrophy and risk of fatal and non-fatal stroke. EUROSTROKE: a collaborative study among research centres in Europe. J Epidemiol Community Health. 2002 Feb;56 Suppl 1(Suppl 1):i8-13.
  32. Bruno A, Brooks DD, Abrams TA, Poorak MD, Gunio D, Kandhal PK, et al. Left ventricular hypertrophy in acute stroke patients with known hypertension. Clin Exp Hypertens [Internet]. 2017;39(6):502–4. Available from: https://doi.org/10.1080/10641963.2016.1259328
  33. Edwards R, Unwin N, Mugusi F, Whiting D, Rashid S, Kissima J, et al. Hypertension prevalence and care in an urban and rural area of Tanzania. J Hypertens. 2000 Feb;18(2):145–52.

Tables

Table 1: Baseline characteristics of the young stroke participants, N=101

Variable

N

%

Female

59

58.4

Mean age±SD

39.7±2

 

Residency

   

  Dar es Salaam

77

76.2

Marital status

   

  Ever married

74

73.3

  Never married

27

26.7

Insured

29

28.7

Medical history

   

  Previous hypertension

66

65.3

  Previous diabetes

13

12.9

  HIV infection

9

8.9

  Ever smoked

6

5.9

  Ever consumed alcohol

23

22.8

Clinical characteristics

   

  NIHSS Mean±SD

18.3±9.2

 

  Systolic blood pressure Mean±SD

153.5±20.1

 

  Diastolic blood pressure Mean±SD

94.5±11.4

 

NIHSS- National institute of health stroke scale, SD- Standard deviation

 

Table 2: Stroke subtype among young stroke participants with and without LVH, N=101

Stroke subtype

LVH n=76 (%)

without LVH n=25 (%)  

Total n=101 (%)

p value

Ischemic

42 (55.3)

18 (72.0)

60 (59.4)

0.139

Hemorrhagic

34 (44.7)

7 (28.0)

41 (40.6)

0.164

 

Table 3: Factors associated with LVH among young stroke participants

Factor

Total

No. with LVH (%)

Unadjusted RR (95% CI)

p value

Adjusted RR (95% CI)

p value

Age group (years)

           

18 - 30

11

45.5

1

 

1

 

31 - 45

90

78.9

1.73 (0.91 - 3.34)

0.10

0.93 (0.52 - 1.64)

0.80

Gender

           

Female

59

72.2

1

     

Male

42

81.0

1.12 (0.91 - 1.42)

0.25

   

Hypertension

           

No

35

62.9

1

 

1

 

Yes

66

81.8

1.30 (1.01 - 1.83)

0.04

0.79 (0.48 - 1.32)

0.37

Not on anti hypertensives

           

No 

27

63.0

1

 

1

 

Yes

39

94.9

1.51 (1.02 - 2.32)

0.01

1.42 (1.04 - 1.94)

0.03

Family history of hypertension

           

No

59

64.4

1

 

1

 

Yes

42

90.5

1.41 (1.14 - 1.74)

0.002

1.13 (0.92 - 1.39)

0.26

Diabetes

           

No

88

75.0

1

     

Yes

13

76.9

1.03 (0.74 - 1.41)

0.88

   

Smoking

           

No

95

74.7

1

     

Yes

6

83.3

1.12 (0.77 - 1.63)

0.57

   

Atrial fibrillation

           

No 

88

75.0

1

     

Yes

3

66.7

0.89 (0.39 - 1.99)

0.78

   

Increased waist-hip ratio

           

No

13

46.2

1

 

1

 

Yes

88

79.5

1.72 (0.95 - 3.13)

0.07

1.22 (0.74 - 2.02)

0.43

Increased LDL

           

No

65

73.8

1

 

1

 

Yes

25

84.0

1.14 (0.95 - 1.46)

0.13

1.03 (0.83 - 1.27)

0.81

Hypercholesteremia

           

No

66

72.7

1

 

1

 

Yes

28

89.3

1.23 (1.05 - 1.55)

0.01

1.08 (0.87 - 1.33)

0.49

  

Table 4: A comparison of 30-day outcomes among young strokes with and without LVH, N=97

 

LVH n=73 (%)

without LVH n= 24 (%)  

Total n=97 (%)

p value

Mortality at 30 days

34 (46.6)

8 (33.3)

42 (43.3)

0.256

Functional independence (mRS 0 - 2)

8 (11.0)

4 (16.7)

12 (12.4)

0.461

mRS- modified Rankin Scale

 

Table 5: The sensitivity and specificity of the electrical voltage criteria in detecting LVH

 

Sokolow-Lyon criteria

Cornell criteria

True positive (n)

18

22

True negative (n)

18

12

False positive (n)

5

11

False negative (n)

50

46

Sensitivity (%) 95% CI

0.27 (0.17 - 0.39)

0.32 (0.22 - 0.45)

Specificity (%) 95% CI

0.78 (0.56 - 0.92)

0.52 (0.31 - 0.73)