Assessment of Diastolic Function

The filling of the ventricle (diastole) is followed by ventricular contraction (systole) to provide an adequate cardiac output during both rest and exercise to meet the body’s metabolic demands. Systole and diastole affect each other in an intimate manner to accomplish this goal. This chapter describes how to determine normal and abnormal left ventricular (LV) filling patterns and to recognize when abnormal LV relaxation, compliance, and filling pressures are present using two-dimensional (2-D) and Doppler technique of mitral and pulmonary venous flow velocity variables. When needed additional information such as color M mode, Doppler tissue imaging, and altering loading conditions help this analysis. By identifying the abnormalities present, and which is predominant, an individualized treatment plan can be devised for cardiac patients.

Restrictive cardiomyopathy (RCM) and constrictive pericarditis (CP) are uncommon cardiac diseases of childhood. RCM is a disease of the myocardium, while CP is a disease of the pericardium; however, they are both diseases of diastolic dysfunction and can present very similarly. Differentiating the two is important because their prognosis and treatment are divergent. This chapter reviews the epidemiology, etiologies, pathology, pathophysiology, clinical presentation, diagnostic evaluation, outcome, and management of pediatric patients with RCM and those with CP.

Restrictive cardiomyopathy (RCM) and constrictive pericarditis (CP) are uncommon cardiac diseases of childhood. RCM is a disease of the myocardium, while CP is a disease of the pericardium; however, they are both diseases of diastolic dysfunction and can present very similarly. Differentiating the two is important because their prognosis and treatment are divergent. This chapter reviews the epidemiology, etiologies, pathology, pathophysiology, clinical presentation, diagnostic evaluation, outcome, and management of pediatric patients with RCM and those with CP.

Pulmonary vein isolation (PVI) has become an accepted therapy for patients with atrial fibrillation (AF) and the indications have widened to include non-paroxysmal AF-patients. Maintenance of sinus rhythm after PVI can be adversely affected by clinical or echocardiographic parameters, which should be clearly identified.

After baseline clinical and echocardiographic evaluations, PVI was performed in patients with paroxysmal or non-paroxysmal AF. The follow-up strategy after PVI included: (1) clinical follow up, 12-lead electrocardiography (ECG) and 24-h ECG every 3 months, (2) trans-telephonic ECGs twice daily and when symptomatic (over 4 weeks) every 3 months, or (3) continuous monitoring via implanted devices. A recurrence was an atrial arrhythmia lasting >30 s. All 340 PVI procedures of 229 patients were analyzed. On average, 1.5 PVI procedures per patient (range, 1–6 PVI) were performed. The mean age was 58 ± 11 years (73% male) with 109 paroxysmal and 120 non-paroxysmal AF cases. Clinical follow-up with 12-lead ECGs, 24-h ECGs, trans-telephonic ECGs, and implanted devices was complete in 100%, 63%, 51%, and 16% of cases, respectively. The overall one-year recurrence rate of 59% (range, 24–82%) was dependent on grades of diastolic function (normal – dysfunction grade III) in a multivariable analysis model. Patients with normal diastolic function had the lowest recurrence rates of 24% and 49% after 1 and 3 years of follow-up, respectively (p < 0.0001).

Diastolic function could serve as a simple summary predictor for AF recurrence, and would facilitate clinical decision-making in AF treatment.

No single well established hypothesis for the mechanisms of heart failure currently exists. Those definitions that do exist are either not universally applicable or are not exclusive to heart failure. The pathogenesis of heart failure has been considered by some to be too complex to define with multiple pathophysiological processes being implicated. The many clinical and neurohumoral features of heart failure may be more dependent on the severity of the condition and its speed of onset rather than its etiology. This suggests a potential single common pathway or pathogenic mechanism in all forms of heart failure regardless of cause.

This viewpoint uses the framework of myocardial mechanics and energetics to propose an alternative, simplified definition and unifying hypothesis for the pathogenesis of chronic heart failure. Chronic heart failure may be understood as follows. Cardiac output and stroke volume are determined by the tissues' requirements; the ejection fraction is determined by both myocardial shortening and degree of end-diastolic wall thickness; the end-diastolic volume is determined by the requirement to normalize stroke volume. We will argue that chronic heart failure can be viewed as a condition where the dominant compensatory mechanism is through regulation of ventricular end-diastolic volume. Consequently, in conditions where there is a fall in tissue perfusion, stroke volume and tissue perfusion are returned toward normal predominantly via this feedback mechanism.

It is important for researchers, clinicians and their patients that we strive for a comprehensive, inclusive and unambiguous unifying hypothesis for pathophysiological mechanisms of heart failure.

Conventional and emerging concepts on mechanisms by which hypertrophic cardiomyopathy (HCM) engenders diastolic dysfunction are surveyed. A shift from familiar left ventricular (LV) diastolic function approaches to large-scale (twist-untwist) and small-scale (titin unfolding-refolding, etc.) wall rebound models, incorporating interaction and dynamic distortions and rearrangements of myofiber sheets and ultrastructural constituents, is suggested. Such an emerging new paradigm of diastolic dynamics, emphasizing the relationship of myofiber sheet and ultraconstituent distortion to LV mechanics and end-systolic shape, might clarify intricate patterns of early diastolic rebound and suction, needed for LV filling in many of the polymorphic phenotypes of HCM.