| ObjectivesOur purposes were to search anatomic method to solve the practical problem that stale hearts after formalin fixation can't be anatomized to ventricular myocardial band(VMB), to further explore the geometric feature and mechanics principle of VMB, based on the research of morphology, to improve the sequential contractile function of VMB and interpret ejection and active filling function of in vivo normal heart, and to investigate the pathological alteration and depressed pumping function of VMB in heart with old myocardial infarction(OMI) and chronic heart failure.Methods and materials1. 20 pig hearts, 20 goat hearts were randomly and respectively divided into 3 groups. Pig heart group 1(PHG1) and sheep heart group 1 (SHG1, n=10, fresh samples without formalin fixation) were dissected by Torrent-Guasp's method, Pig heart group 2 (PHG2) and sheep heart group 2 (SHG2 n=5, stale samples over 1 month after formalin fixation) were dissected by Torrent-Guasp's method, Pig heart group 3 (PHG3) and sheep heart group 3 (SHG3, n=5, stale samples over 1 month after formalin fixation) were dissected by new method. 2 human hearts over 6 months after formalin fixation were dissected by new method.2. Ex vivo pig hearts (n=10), goat hearts(n=10) and dog hearts(n=10) after preparation were detected by MR diffusion tensor imaging (MRDTI) in which fiber tracking and artificial color were performed to observe the myofibrillar spatial trajectory and the crossing angle (CA) of descending segment (DS) and ascending segment(AS). The length percentage of each segment and apical division proportion (ADP) between DS and AS were measured.3. Healthy male dogs (n=10) underwent thoracotomy in which tin beads were placed into myocardium based on the spatial trajectory of VMB. At the first, second, third week after surgery, the movement of tin beads were recorded by digital subtraction centiography (DSC).4. Healthy male dogs (n=5) underwent the same operation as above protocol. 2 weeks latter, the animals underwent thoracotomy again and they suffered from acute anterior wall infarction after their left anterior descending artery (LAD) was ligated.At the first, second month after myocardial infarction, the movement of tin beads were recorded by DSC. MRDTI and anatomy of VMB were performed after the animals sacrificed. ADP and infarct area percentage (IAP) of DS and AS were measured.5. Healthy male dogs (n=5) underwent the same operation as in the above mentioned protocol. 2 weeks latter, the animals whose VMB had been marked by tin beads underwent rapid ventricular pacing (RVP, 230 times/minute). At the second, third week after RVP, the movement of tin beads were recorded by DSC. MRDTI and anatomy of VMB were performed after the animals were sacrificed, ADP and CA were measured.Results1. By Torrent-guasp' method, all fresh samples in PHG1 and SHG1 were successfully unrolled to VMB, but all stale samples after formalin fixation were not. On the contrary, by the new method, all samples (PHG3, SHG3 and human hearts) after formalin fixation were successfully dissected to VMB. Furthermore, clear myofibrillar trajectory and CA were discovered.2. Double coiled spiral structure of myocardial fiber and near vertical crossing between DS and AS were found in MRDTI.There weren't significant difference at the length percentage same segment in the hearts in different species (P>0.05). There wasn't significant difference between ADP and gold division proportion(P>0.05).3. Generally speaking, cardiac movement presented a sequential process from narrowing to shortening, to lengthening, and to widening. Partially speaking, the following sequence was observed. Basal loop originated shortening at earliest stage, DS closely followed it, and AS initiated shortening at latest moment (P<0.01). The descending segment stops shortening during the rapid filling phase of fast descent of ventricular pressure, but AS stopped shortening at later moment (40-80ms) than DS, so that active shortening continues during the period of isovolumetric relaxation.4. Functionally, the following sequence of cardiac contraction disappeared and the whole and regional function of systole and diastole significantly decreased in hearts with OMI. Morphologically, the impairment of AS was more serious than that of DS, the IAP in AS was significantly greater than that in DS (P<0.01), and the ADP was significantly lower than gold division proportion in hearts with OMI (P< 0.01)..5. Functionally, the whole and regional function of systole and diastolesignificantly decreased in hearts with CHF(P<0.01), and the function of apical loop was impaired most seriously (P<0.001), Morphologically, CA of DS and AS significantly increased (P<0.01), and the ADP was significantly lower gold than division proportion in hearts with CHF (P<0.01). Conclusion1. Our new method achieved the first time anatomy of VMB in hearts after formalin fixation. This is a supplement to the Torrent-Guasp's method and solves the big problem that stale hearts after formalin fixation can't be anatomized to VMB. This establishes the basis of methodology and sample resource for supporting widespread study on clinical application of VBM theory.2. Our study objectively proved the existence of Double coiled spiral structure of VMB in the heart. We exactly measured crossing angle of DA and AS on the first time, discovered the rule of ADP equaling to gold division in VMB. These geometric features are the material basis of pumping function in the heart. Abnormal crossing of any causes will impair the pumping function of the heart.3. Our study firmly supports Torrent-Guasp's hypothesis on sequential contraction of the heart. It is the functional reflection of the helical VMB. DS shortening is responsible for cardiac twist and quick ejection. On the other hand, the delayed contraction of AS results in cardiac untwisting and active filling.4. It is the first time that we discover the pathology that there are more impaired quantity and quality in AS than that in DS in the heart with OMI. This reveals the mechanism of impaired diastolic function in heart with anterior wall infarction. Postinfarcted ventricular remodeling (PIVR) causes the deviation of ADP from gold division, which breaks down the stability of double coiled spiral structure of VMB in heart. This makes the possibility of decompensated cardiac dilatation and CHF.5. Our study achieves the first time observation of more transverse fiber orientation in apical loop and abnormal crossing angle of AS and DS in helical VMB in the heart with CHF. This potentially is the mechanism that cardiac ejection and filling are impaired in the heart with CHF. |
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