Changes in left ventricular volume, mass, and function during the development and regression of supraventricular tachycardia-induced cardiomyopathy. Disparity between recovery of systolic versus diastolic function.

Tomita, Masaaki; Spinale, Francis G.; Crawford, Fred A.; Zile, Michael R.

doi:10.1161/01.cir.83.2.635

Cited by 147 publications

(65 citation statements)

References 36 publications

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“…[1][2][3][4][5][6][7][8][9] In addition, changes in Figure 3. Zymographic activity was computed with linear scans of the digitized gelatin zymograms and the densitometric profiles converted into pixels.…”

Section: Discussionmentioning

confidence: 99%

“…1,3,4 These clinical observations as well as experimental studies suggest that LV remodeling is an important contributory event in the progression to end-stage DCM. [5][6][7][8][9] However, the structural basis and contributory mechanisms for the changes in LV geometry that occur during the progression of DCM remain unclear. An important constituent of the LV myocardium is the fibrillar collagen matrix, which contributes to the maintenance of LV geometry and the structural alignment of adjoining myocytes.…”

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confidence: 99%

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Increased Matrix Metalloproteinase Activity and Selective Upregulation in LV Myocardium From Patients With End-Stage Dilated Cardiomyopathy

et al. 1998

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Background-One of the hallmarks of dilated cardiomyopathy (DCM) is left ventricular (LV) remodeling. The matrix metalloproteinases (MMPs) are a family of enzymes that contribute to extracellular remodeling in several disease states. Additionally, a family of inhibitors called tissue inhibitors of MMPs (TIMPs) has been shown to exist and to tightly regulate MMP activity. However, the types of MMPs and TIMPs expressed within the normal and DCM LV myocardium and the relation to MMP activity remain unexplored. Methods and Results-Relative LV myocardial MMP activity was determined in the normal (nϭ8) and idiopathic DCM (nϭ7) human LV myocardium by substrate zymography. Relative LV myocardial abundance of interstitial collagenase (MMP-1), stromelysin (MMP-3), 72 kD gelatinase (MMP-2), 92 kD gelatinase (MMP-9), TIMP-1, and TIMP-2 were measured with quantitative immunoblotting. LV myocardial MMP zymographic activity increased with DCM compared with normal (984Ϯ149 versus 413Ϯ64 pixels, PϽ.05). With DCM, LV myocardial abundance of MMP-1 decreased to 16Ϯ6% (PϽ.05), MMP-3 increased to 563Ϯ212% (PϽ.05), MMP-9 increased to 422Ϯ64% (PϽ.05), and MMP-2 was unchanged when compared with normal. LV myocardial abundance of TIMP-1 and TIMP-2 increased by Ͼ500% with DCM. A high-molecular-weight immunoreactive band for both TIMP-1 and TIMP-2, suggesting a TIMP/MMP complex, was increased Ͼ600% with DCM. Conclusions-This study demonstrated increased LV myocardial MMP activity and evidence for independent regulatory mechanisms of MMP and TIMP expression with DCM. These findings suggest that selective inhibition of MMP species within the LV myocardium may provide a novel therapeutic target in patients with DCM.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Increased Matrix Metalloproteinase Activity and Selective Upregulation in LV Myocardium From Patients With End-Stage Dilated Cardiomyopathy

et al. 1998

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“…33,[38][39][40]44 LV dilation is more marked for end-systolic than end-diastolic volumes, 41,42 and produces a spherical chamber geometry. 38,39,54 Commonly, left ventricular cavity dilation is accompanied by little or no change in LV wall mass with a normal or reduced LV wall thickness. 22,39 Cellular changes accompanying the change in chamber size include cellular elongation, decreased myocyte cross-sectional area and disruption of normal myofibril alignment.…”

Section: Structural Changesmentioning

confidence: 99%

What About Tachycardia-induced Cardiomyopathy?

Ellis¹,

Josephson²

2013

Arrhythmia &Amp; Electrophysiology Review

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Cardiomyopathies are heterogeneous heart muscle disorders with a wide range of aetiologies and clinical manifestations. They are often defined by their causes (i.e. hypertension, prior myocardial infarction, valvular heart disease), although current major society definitions describe cardiomyopathy as the presence of abnormal myocardial structure and/or function in the absence of underlying structural heart disease. Long-standing tachycardia is a well-recognised cause of heart failure and left ventricular dysfunction, and has led to the nomenclature, tachycardia-induced cardiomyopathy (TIC). TIC is generally a reversible cardiomyopathy if the tachycardia can be treated effectively, either with medications, surgery or catheter ablation. TIC can also manifest in patients with baseline left ventricular dysfunction from underlying structural heart disease that develop a worsening of their myocardial dysfunction in the setting of prolonged tachycardia, which can be reversed with control of the tachycardia. The diagnosis is usually made after demonstrating recovery of left ventricular function with normalisation of heart rate in the absence of other identifiable aetiologies.TIC was first described in 1913 in a young patient who presented with congestive heart failure (CHF) and atrial fibrillation (AF) with rapid ventricular response.1 In the subsequent decades, further reports were written documenting cases of complete resolution of CHF after cardioversion of AF to sinus rhythm.2-4 A century after the first reported case, we are still working to expand our understanding of the mechanisms underlying this disorder. A variety of chronic or incessant tachyarrhythmias have been implicated in the pathogenesis of TIC, the most classic being AF, 5-7 atrial flutter, 8 incessant supraventricular tachycardia, 9-12 ventricular tachycardia [13][14][15][16] and premature ventricular depolarizations 17 (see Table 1). The most common presentation is a dilated cardiomyopathy with or without the causative tachycardia.Given that this diagnosis represents a potentially reversible cause of heart failure, its recognition is critically important. In this review, we will discuss the proposed mechanisms of TIC, the causative tachycardias and their treatment, outcomes for patients diagnosed with TIC, and future directions for research and clinical care. Experimental Models BackgroundThe first experimental model of TIC was described by Whipple et al. in 1962 where he demonstrated that rapid, prolonged atrial pacing resulted in low output heart failure.18 This model has since become widely used as a model to study CHF. Animal studies, primarily in dogs and pigs, have shown that sustained rapid atrial or ventricular pacing results in systolic heart failure that is neurohormonally and haemodynamically similar to left ventricular systolic dysfunction in humans. [19][20][21][22][23] The majority of what is known about the pathophysiologic mechanisms underlying TIC is supported by pacing-induced heart failure in animal models (see Table 2). It is ...

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“…These methods have been described previously in detail. 5,33 Echocardiographic data were measured according to the American Society of Echocardiography criteria,34 including the leading edge convention. End diastole was defined at the Q wave of the ECG.…”

Section: Simultaneous LV Echocardiography and Catheterizationmentioning

confidence: 99%

Changes in diastolic function during development and correction of chronic LV volume overload produced by mitral regurgitation.

et al. 1993

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Background. Mitral regurgitation (MR) causes an augmentation in left ventricular (LV) diastolic function, increasing early diastolic filling rate and decreasing LV stiffness. Whether these changes in diastolic function persist, return to normal, or become abnormal after mitral valve replacement (MVR) is unknown.Methods and Results. Simultaneous LV echocardiography and catheterization studies were performed in six dogs in the baseline state (baseline), 3 months after creation of MR (chronic MR), and 3 months after MVR. Chronic MR caused LV dilation (end-diastolic dimension increased from 4.5±0.1 cm in baseline to 5.8+0.1 cm in chronic MR,p<0.05) and eccentric LV hypertrophy (LV-to-body weight ratio increased from 3.6±0.2 g/kg in baseline to 4.9±0.4 g/kg in chronic MR, p<0.05). Chronic MR caused an increase in LV early diastolic filling rate (peak rate of increase in minor-axis dimension increased from 11±1 cm/sec in baseline to 18+1 cm/sec in chronic MR,p<0.05), did not change the time constant of myocardial relaxation (T was 31±4 msec in baseline and 30±2 msec in chronic MR), and caused a decrease in the modulus of regional chamber stiffness from 7.7± 1.2 in baseline to 2.4±0.03 in chronic MR,p<0.05. MVR caused the resolution of LV dilation (end-diastolic dimension returned to normal [4.8±0.2 cm]), but three months after MVR, regression of LV hypertrophy was incomplete (LV-to-body weight ratio remained

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Changes in left ventricular volume, mass, and function during the development and regression of supraventricular tachycardia-induced cardiomyopathy. Disparity between recovery of systolic versus diastolic function.

Cited by 147 publications

References 36 publications

Increased Matrix Metalloproteinase Activity and Selective Upregulation in LV Myocardium From Patients With End-Stage Dilated Cardiomyopathy

Increased Matrix Metalloproteinase Activity and Selective Upregulation in LV Myocardium From Patients With End-Stage Dilated Cardiomyopathy

What About Tachycardia-induced Cardiomyopathy?

Changes in diastolic function during development and correction of chronic LV volume overload produced by mitral regurgitation.

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