No abstract

Abstract-The keynote to understanding cardiac function is recognizing the underlying architecture responsible for the contractile mechanisms that produce the narrowing, shortening, lengthening, widening, and twisting disclosed by echocardiographic and magnetic resonance technology. Despite background knowledge of a spiral clockwise and counterclockwise arrangement of muscle fibers, issues about the exact architecture, interrelationships, and function of the different sets of muscle fibers remain to be resolved. This report (1) details observed patterns of cardiac dynamic directional and twisting motions via multiple imaging sources; (2) summarizes the deficiencies of correlations between ventricular function and known ventricular muscle architecture; (3) correlates known cardiac motions with the functional anatomy within the helical ventricular myocardial band; and (4) defines an innovative muscular systolic mechanism that challenges the previously described concept of "isovolumic relaxation Key Words: diastole Ⅲ heart failure Ⅲ muscles Ⅲ ventricles C ongestive heart failure, due usually to both left ventricular (LV) and right ventricular failure, is an increasing problem worldwide. In the United States, Ϸ5 million patients suffer from congestive heart failure, and each year Ϸ500 000 new patients develop the condition. 1 Originally, this syndrome was believed to be due to failure of the LV to pump blood efficiently (ie, systolic ventricular failure). More recently, emphasis has been placed on diastolic ventricular failure, in which systolic function appears to be normal but diastolic ventricular function is impaired. 2-4 Diastolic dysfunction, in fact, may be the cause of congestive heart failure in up to 50% of these patients. 5,6 We have had treatment for systolic ventricular failure for many years, even if it is imperfect; at present, however, no agreement has been reached about the best ways of treating diastolic ventricular failure. To develop better treatments for congestive heart failure, both systolic and diastolic, we need first to understand the basic physiology of normal and abnormal ventricular contraction and relaxation.The heart is a muscular pump that supplies blood to the body. This goal is achieved by electric excitation that produces sequential ventricular emptying and filling. Figure 1a demonstrates the physiological sequence of ventricular function: an isovolumic contraction phase to develop preejection tension, ejection, a postejection isovolumic phase, and then rapid and slow periods for filling. LV volume decreases rapidly early in systole and slowly thereafter, corresponding to the rapid early acceleration in the flow curve. The volume then increases rapidly in early filling and more slowly during late filling.The information shown in Figure 1a is still correct, but it is only slightly more informative than the concept of William Harvey, who concluded, after dissecting cadaver hearts, that the heart squeezed by constriction to eject and dilated passively to fill. This accepted view of car...

Ventricular torsion and untwisting are essential for normal ventricular function and their mechanisms are related to the temporal responses of the helical and circular muscle fibers that comprise cardiac architecture. Explanation of the presystolic isovolumic contraction (IVC) period is essential for analysis of these interactions. Structural and imaging studies by magnetic resonance, speckle tracking, velocity vector encoding, and sonomicrometer crystals are described to define why and how different muscular components contract asynchronously. Mechanical and functional relationships are described for pre-systolic IVC, torsion, postejection isovolumic interval, and rapid and slow filling. Circular fibers dominate to cause pre- and posttwisting global counterclockwise and clockwise movement, and helical fibers govern torsion whereby the base rotates clockwise and apex counterclockwise; untwisting cannot begin until torsion is completed. Prolonged torsion extends into the postejection isovolumic interval and delays untwisting, and is caused by prolonged contraction of the right-handed helical arm or descending segment of the helical ventricular myocardial band that narrows the ∼80 ms "timing hiatus" between end of shortening of the descending and the ascending segment or left-handed arm of the helical muscle. Longer torsion duration by this mechanism becomes the common theme for unbalanced torsion and untwisting in diastolic dysfunction, physiological, structural, and electrical disease processes, whose management may be guided by changing the interconnected reasons for these adverse mechanical and timing factors.

Further testing of these spatial anatomic concepts is needed to create a more accurate understanding of the architectural mechanisms that underlie cardiac dynamics to address future problems in unhealthy hearts.

Mental stress in the laboratory results in a substantial sympathetic response in normal middle-aged and older men and women, but EF commonly falls because of a concomitant rise in afterload. These results provide essential age- and sex-matched reference data for studies of mental stress-induced ischemia in patients with coronary artery disease.