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  1. Azarisman SM, Carbone A, Shirazi M, Bradley J, Teo KS, Worthley MI, et al.
    Heart Lung Circ, 2016 Nov;25(11):1094-1106.
    PMID: 27210302 DOI: 10.1016/j.hlc.2016.03.011
    BACKGROUND: Cardiovascular magnetic resonance (CMR) advances in imaging techniques, permits the ability to accurately characterise tissue injury post myocardial infarction. Pre-contrast T1 mapping enables this through measurement of pre-contrast T1 relaxation times. We investigate the relationship between T1 characterisation of myocardial injury with global and regional diastolic function.

    METHODS: Revascularised acute myocardial infarction patients with normal left ventricular (LV) systolic function on TTE were assessed by 1.5T CMR. Acute regional diastolic wall motion abnormalities, global diastolic function measurements, acute segmental damage fraction with LGE and mean segmental pre-contrast T1 values were assessed on matching short axis slices.

    RESULTS: Forty-four patients were analysed. Mean LVEF was 62.1±9.4%. No difference between NSTEMI (22/44) and STEMI in mean pre-contrast T1 values of infarcted (1025.0±109.2 vs 1011.0±81.6ms, p=0.70), adjacent (948.3±45.3 vs 941.1±46.6ms, p=0.70) and remote (888.8±52.8 vs 881.2±54.5ms, p=0.66) segments was detected. There was no correlation between pre-contrast T1 of infarcted segments with global diastolic dysfunction (E/A, r(2)=0.216, p=0.06; S/D, r(2)=0.243, p=0.053; E/E', r(2)=0.240, p=0.072), but there was significantly positive, moderate correlation with circumferential diastolic strain rate, (r(2)=0.579, p<0.01) with excellent agreement and reproducibility.

    CONCLUSION: Cardiac magnetic resonance evaluation of pre-contrast T1 values revealed no difference between NSTEMI and STEMI patients in terms of tissue characterisation post-myocardial infarction. However, pre-contrast T1 of infarcted tissue is significantly correlated with regional diastolic circumferential strain rate.

    Matched MeSH terms: Ventricular Dysfunction, Left/etiology
  2. Jeyamalar R, Chan SP
    Int J Cardiol, 1995 Nov 10;52(1):83-4.
    PMID: 8707441
    Thyrotoxicosis gives rise to a high output cardiac failure. Rarely, it can cause a dilated cardiomyopathy with severe impairment of myocardial function which improves significantly following treatment.
    Matched MeSH terms: Ventricular Dysfunction, Left/etiology
  3. Abdul Aziz KA, Draman N, Wan Isa WYH, Mustaffa N
    Med J Malaysia, 2020 07;75(4):396-399.
    PMID: 32724001
    Cirrhotic cardiomyopathy is a recognised complication of liver cirrhosis and predicts poor outcomes. Detection of diastolic dysfunction, an early indicator of left ventricular dysfunction can help identify those patients at risk of disease progression. In our study we showed that there was a high prevalence of diastolic dysfunction amongst patients with liver cirrhosis at our outpatient clinic, with the majority being Child-Pugh A/low MELD score. Multiple regression analysis indicated that age and sodium levels were significantly associated with the presence of diastolic dysfunction. This further reinforces the importance of dietary sodium restriction amongst patients with liver cirrhosis.
    Matched MeSH terms: Ventricular Dysfunction, Left/etiology*
  4. Fang F, Luo XX, Zhang Q, Azlan H, Razali O, Ma Z, et al.
    Europace, 2015 Oct;17 Suppl 2:ii47-53.
    PMID: 26842115 DOI: 10.1093/europace/euv130
    Biventricular (BiV) pacing was superior to right ventricular apical (RVA) pacing at extended follow-up in the Pacing to Avoid Cardiac Enlargement (PACE) trial. Early pacing-induced systolic dyssynchrony (DYS) might be related to mid-term result. However, it remains unknown whether early pacing-induced DYS can predict long-term reduction of left ventricular (LV) systolic function.
    Matched MeSH terms: Ventricular Dysfunction, Left/etiology*
  5. Salamonsen RF, Lim E, Moloney J, Lovell NH, Rosenfeldt FL
    Artif Organs, 2015 Aug;39(8):681-90.
    PMID: 26146861 DOI: 10.1111/aor.12550
    This study in five large greyhound dogs implanted with a VentrAssist left ventricular assist device focused on identification of the precise site and physiological changes induced by or underlying the complication of left ventricular suction. Pressure sensors were placed in left and right atria, proximal and distal left ventricle, and proximal aorta while dual perivascular and tubing ultrasonic flow meters measured blood flow in the aortic root and pump outlet cannula. When suction occurred, end-systolic pressure gradients between proximal and distal regions of the left ventricle on the order of 40-160 mm Hg indicated an occlusive process of variable intensity in the distal ventricle. A variable negative flow difference between end systole and end diastole (0.5-3.4 L/min) was observed. This was presumably mediated by variable apposition of the free and septal walls of the ventricle at the pump inlet cannula orifice which lasted approximately 100 ms. This apposition, by inducing an end-systolic flow deficit, terminated the suction process by relieving the imbalance between pump requirement and delivery from the right ventricle. Immediately preceding this event, however, unnaturally low end-systolic pressures occurred in the left atrium and proximal left ventricle which in four dogs lasted for 80-120 ms. In one dog, however, this collapse progressed to a new level and remained at approximately -5 mm Hg across four heart beats at which point suction was relieved by manual reduction in pump speed. Because these pressures were associated with a pulmonary capillary wedge pressure of -5 mm Hg as well, they indicate total collapse of the entire pulmonary venous system, left atrium, and left ventricle which persisted until pump flow requirement was relieved by reducing pump speed. We suggest that this collapse caused the whole vascular region from pulmonary capillaries to distal left ventricle to behave as a Starling resistance which further reduced right ventricular output thus contributing to a major reduction in pump flow. We contend that similar complications of manual speed control also occur in the human subject and remain a major unsolved problem in the clinical management of patients implanted with rotary blood pumps.
    Matched MeSH terms: Ventricular Dysfunction, Left/etiology*
  6. Aslannif R, Suraya K, Koh HB, Tey YS, Tan KL, Tham CH, et al.
    Med J Malaysia, 2019 12;74(6):521-526.
    PMID: 31929479
    INTRODUCTION: Apical Hypertrophic Cardiomyopathy (Apical HCM) is an uncommon variant of hypertrophic cardiomyopathy, but it is relatively more common in Asian countries. This is a retrospective, non-randomised, single centre study of patients with Apical HCM focusing on their diastolic dysfunction grading, echocardiographic parameters and electrocardiograms (ECG).

    METHODS: All Apical HCM patients coming for clinic visits at the Institut Jantung Negara from September 2017 to September 2018 were included. We assessed their echocardiography images, grade their diastolic function and reviewed their ECG on presentation.

    RESULTS: Fifty patient were included, 82% (n=41) were males and 18% (n=9) females. The diastolic function grading of 37 (74%) patients were able to be determined using the updated 2016 American Society of Echocardiography (ASE) diastolic guidelines. Fifty percent (n=25) had the typical ace-ofspades shape left ventricle (LV) appearance in diastole and 12% (n=6) had apical pouch. All patients had T inversion in the anterior leads of their ECG, and only 52% (n=26) fulfilled the ECG left ventricular hypertrophy (LVH) criteria. Majority of our patients presented with symptoms of chest pain (52%, n=26) and dyspnoea (42%, n=21).

    CONCLUSION: The updated 2016 ASE guideline makes it easier to evaluate LV diastolic function in most patients with Apical HCM. It also helps in elucidating the aetiology of dyspnoea, based on left atrial pressure. Clinicians should have a high index of suspicion for Apical HCM when faced with deep T inversion on ECG, in addition to a thick LV apex with an aceof- spades appearance during diastole.

    Matched MeSH terms: Ventricular Dysfunction, Left/etiology
  7. Lum LC, Chua KB, McMinn PC, Goh AY, Muridan R, Sarji SA, et al.
    J Clin Virol, 2002 Jan;23(3):153-60.
    PMID: 11595594
    Hand, foot, and mouth disease (HFMD) is endemic in Malaysia. In 1997, a large outbreak of enterovirus 71 (EV-71) associated HFMD resulted in 41 deaths due to severe left ventricular dysfunction and central nervous system infection with extensive damage to the medulla and pons. The clinical presentation in all these patients were rapid cardio-respiratory decompensation leading to cardiac arrest. Another large outbreak of HFMD with 55 fatal cases and a similar clinical picture was reported in Taiwan in 1998. In 2000, an outbreak of HFMD resulted in the deaths of three children who had rapid cardio-respiratory decompensation and one child who survived a central nervous system infection.
    Matched MeSH terms: Ventricular Dysfunction, Left/etiology
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