Effect of angiotensin-converting enzyme inhibitors on non-diseased myocardium of experimental animals: potential clinical implications

Angiotensin-converting enzyme (ACE) inhibitors protect the hearts of patients with different levels of cardiac disorder. The greatest benefit seems to be achieved in subjects with most severe heart failure. Moreover, ACE inhibition is protective also in patients without manifested heart failure but with severe systolic left ventricular dysfunction. Data are presented that ACE inhibitors can alter the composition of the myocardium also in control: healthy animals. In rats and rabbits with non-diseased heart, chronic ACE inhibition reduced fibrotic tissue concentration in the left ventricle. We speculate that if this were applied to humans, ACE inhibition may prove to be of potential benefit in subjects with normal systolic function but with a trend to left ventricular filling abnormalities caused by increased ventricular stiffness. In these patients reduction of myocardial fibrotic tissue might prevent deterioration of diastolic function.     

Simulation of cardiovascular physiology: the diastolic function(s) of the heart

The cardiovascular system was simulated by using an equivalent electronic circuit. Four sets of simulations were performed. The basic variables investigated were cardiac output and stroke volume. They were studied as functions (i) of right ventricular capacitance and negative intrathoracic pressure; (ii) of left ventricular relaxation and of heart rate; and (iii) of left ventricle failure. It seems that a satisfactory simulation of systolic and diastolic functions of the heart is possible. Presented simulations improve our understanding of the role of the capacitance of both ventricles and of the diastolic relaxation in cardiovascular physiology.     

Acute aortocaval fistula: role of low perfusion pressure and subendocardial remodeling on left ventricular function

The experimental model of aortocaval fistula is a useful model of cardiac hypertrophy in response to volume overload. In the present study it has been used to investigate the pathologic subendocardial remodeling associated with the development of heart failure during the early phases (day 1, 3, and 7) following volume overload. Compared with sham treated rats, aortocaval fistula rats showed lower systemic blood pressure and higher left ventricular end‐diastolic pressure This resulted in lower coronary driving pressure and left ventricular systolic and diastolic dysfunction. Signs of myocyte necrosis, leukocyte cell infiltration, fibroplasia and collagen deposition appeared sequentially in the subendocardium where remodeling was more prominent than in the non‐subendocardium. Accordingly, increased levels of TNF‐alpha, IL‐1 beta, and IL‐6, and enhanced MMP‐2 activity were all found in the subendocardium of rats with coronary driving pressure ≤60 mmHg. The coronary driving pressure was inversely correlated with MMP‐2 activity in subendocardium in all time‐points studied, and blood flow in this region showed positive correlation with systolic and diastolic function at day 7. Thus the predominant subendocardial remodeling that occurs in response to low myocardial perfusion pressure during the acute phases of aortocaval fistula contributes to early left ventricular dysfunction.     

Functional changes in left ventricular hypertrophy: diagnosis of impaired diastolic function in patients with hypertension

Summary Left ventricular hypertrophy is usually associated with impaired left ventricular diastolic function which can be characterised by an altered pressure volume relationship. Since diastolic flow velocities are closely related to the difference in pressure between the left atrium and left ventricle, parameters of diastolic function can be determined by Doppler echocardiography. However, the pressure difference is additionally influenced by factors which have no relation to left ventricular diastolic function. These include preload, afterload, inotropy, heart rate and left ventricular systolic function. Despite these limitations, Doppler echocardiography is a valuable tool to diagnose therapeutic effects on diastolic function in patients with left ventricular hypertrophy.     

频谱多谱勒技术评价冠心病人心室舒张功能

目的：采用频谱多谱勒技术观察冠心病人心室舒张功能改变。方法：冠状动脉造影确诊为冠心病患者61例，根据左室射血分数（EF）分为EF正常组（Ⅰ组，EF≥50％，33例），EF降低组（Ⅱ组，EF〈50％，28例）。正常对照组32例。频谱脉冲多普勒技术测量各组二尖瓣、三尖瓣血流频谱及肺静脉血流频谱参数；心导管测量冠心病组左室舒张末压（LVEDP）。结果：冠心病Ⅰ组左、右室舒张功能均可出现障碍，多呈松弛功能异常；冠心病Ⅱ组左室舒张功能障碍，多呈假性正常化；PVad-Ad与LVEDP呈正相关（r=0．72，P〈0．01）；以PVad-Ad〉0ms为标准来鉴别二尖瓣频谱假性正常化，敏感性为92％，特异性为80％；左右室舒张功能相关性分析（E／A：r=0．46，DT：r=0．54，P〈0．01）。结论：冠心病早期收缩功能正常时，左、右室舒张功能均可出现障碍；左室收缩功能异常时，左室舒张功能进一步减退，多呈假性正常化；PVad-Ad能准确地鉴别二尖瓣血流频谱假性正常化；冠心病人左右室舒张功能有较显著的相关性。     

The effects of asymmetric ventricular filling on left–right ventricular interaction in the normal rat heart

Heart failure is characterised by ventricular dysfunction and with the potential for changes to ventricular volumes constraining the mechanical performance of the heart. The contribution of this interaction from geometric changes rather than fibrosis or metabolic changes is unclear. Using the constant pressure Langendorff-perfused rat heart, the volume interaction between left ventricle (LV) and right ventricle (RV) was investigated. RV diastolic stiffness (P?<?0.001) and developed pressure (P?<?0.001) were significantly lower than LV. When the RV was fixed at the end-diastolic volume (EDV) or EDV?+?50?%, both LV systolic and diastolic performance were unaffected with increasing LV balloon volume. However, at fixed LV volume, RV systolic performance was significantly decreased when LV volume increased to EDV?+?50?% when RV volume was increased incrementally between 50 and 300?μl (P?<?0.001). Systolic interaction in RV was noted as declining RV peak systolic load with increasing LV systolic pressure (P?<?0.05) and diastolic interaction was noted for RV when LV volume was increased from EDV to EDV?+?50?% (P?<?0.05). RV diastolic wall stress was increased with increasing LV balloon volume (P?<?0.05), but LV wall stress was unaltered at fixed RV balloon volume. Taken together, increasing LV volume above EDV decreased systolic performance and triggered ventricular constraint in the RV but the RV itself had no effect on the performance of the LV. These results are consistent with overload of the LV impairing pulmonary perfusion by direct ventricular interaction with potential alteration to ventilation–perfusion characteristics within the lung.     

Myocyte cellular hypertrophy and hyperplasia contribute to ventricular wall remodeling in anemia-induced cardiac hypertrophy in rats.

To determine the effects of chronic anemia on the functional and structural characteristics of the heart, 1-month-old male rats were fed a diet deficient in iron and copper, which led to a hemoglobin concentration of 4.63 g/dl, for 8 weeks. At sacrifice, under fentanyl citrate and droperidol anesthesia, systolic, diastolic, and mean arterial blood pressures were decreased, whereas differential pressure was increased. Left ventricular systolic pressure and the ventricular rate of pressure rise (mmHg/s) were reduced by 9% and 14%, respectively. Moreover, developed peak systolic ventricular pressure and maximal dP/dt diminished 14% and 12%. After perfusion fixation of the coronary vasculature and the myocardium, at a left ventricular intracavitary pressure equal to the in vivo measured end diastolic pressure, a 10% thickening of the left ventricular wall was measured in association with a 13% increase in the equatorial cavitary diameter and a 44% augmentation in ventricular mass. The 52% hypertrophy of the right ventricle was characterized by an 11% thicker wall and a 37% larger ventricular area. The 33% expansion in the aggregate myocyte volume of the left ventricle was found to be due to a 14% myocyte cellular hypertrophy and a 17% myocyte cellular hyperplasia. These cellular parameters were calculated from the estimation of the number of myocyte nuclei per unit volume of myocardium in situ and the evaluation of the distribution of nuclei per cell in enzymatically dissociated myocytes. Myocyte cellular hyperplasia provoked a 9% increase in the absolute number of cells across the left ventricular wall. In contrast, myocyte cellular hypertrophy (42%) was responsible for the increase in myocyte volume of the right ventricle. The proliferative response of left ventricular myocytes was not capable of restoring diastolic cell stress, which was enhanced by the changes in ventricular anatomy with anemia. In conclusion, chronic anemia induced an unbalanced load on the left ventricle, which evoked a hyperplastic reaction of preexisting myocytes, in an attempt to normalize diastolic wall and myocyte stress.     

Renin-angiotensin system and myocardial collagen matrix remodeling in hypertensive heart disease: in vivo and in vitro studies on collagen matrix regulation

Summary The interstitial space of the myocardium is composed of nonmyocyte cells and a highly organized collagen network which serves to maintain the architecture and mechanical behavior of the myocardial walls. It is the myocardial collagen matrix that determines myocardial stiffness in the normal and structurally remodeled myocardium. In hypertensive heart disease, the heterogeneity in myocardial structure, created by the altered behavior of nonmyocyte cells, particularly cardiac fibroblasts which are responsible for collagen synthesis and degradation, explains the appearance of diastolic and/or systolic dysfunction of the left ventricle that leads to symptomatic heart failure. Several lines of evidence suggest that circulating and myocardial renin-angiotensin systems (RAS) are involved in the regulation of the structural remodeling of the nonmyocyte compartment, including the cardioprotective effects of angiotensin converting enzyme (ACE) inhibition that was found to prevent myocardial fibrosis in the rat with renovascular hypertension. In cultured adult rat cardiac fibroblasts angiotensin II was shown to directly stimulate collagen synthesis and to inhibit collagenase activity, which is the key enzyme for collagen degradation, that would lead to collagen accumulation. In the spontaneously hypertensive rat, an appropriate experimental model for primary hypertension in man, left ventricular hypertrophy could be regressed and abnormal myocardial diastolic stiffness due to interstitial fibrosis could be restored to normal by inhibition of the myocardial RAS. These antifibrotic or cardioreparative effects of ACE inhibition that occurred irrespective of blood pressure normalization may be valuable in reversing left ventricular diastolic dysfunction in hypertensive heart disease.     

Large animal models for diastolic dysfunction and diastolic heart failure—a review of the literature

Diastolic heart failure (DHF) or heart failure with preserved systolic left ventricular function is estimated to account for approximately 40% of heart failure cases. Medical treatment of patients with DHF is limited and mainly empirical. Device-based therapy has an increasing role in the treatment of systolic heart failure and may have a future role in the treatment of DHF patients. Diastolic dysfunction and DHF are associated with anatomical and physiological characteristics, which need to be modeled in large animals in order to allow evaluation of device-based therapies, prior to clinical studies. In this article, we will review the large animal models for diastolic dysfunction and heart failure.     

不同β-肾上腺素能受体对低氧应激大鼠心脏舒缩功能的影响

目的:探讨不同β-肾上腺素能受体(β-adrenergic receptor,β-AR)在急性低氧应激中对大鼠左、右心室舒缩功能的影响。方法:健康雄性SD大鼠随机分为4组(n=7):对照组(control group)、非选择性β-肾上腺素能受体阻断剂普萘洛尔组(propranolol group)、选择性β_1-肾上腺素能受体阻断剂阿替洛尔组(atenolol group)和选择性β2-肾上腺素能受体阻断剂ICI 118,551组(ICI 118,551 group),各组大鼠分别在常氧(西宁,海拔2 260 m,20.9% O_2,79.1% N_2)和急性低氧(15.0% O_2,85.0% N_2)通气的状态下进行实验,监测各组大鼠心率(heart rate,HR)、左心室收缩压(left ventricular systolic pressure,LVSP)、右心室收缩压(right ventricular systolic pressure,RVSP)及左、右心室内压最大上升和下降速率(±dp/dt_(max))等心功能指标变化;同时,比较低氧通气前后动脉血气的变化。结果:常氧下,propranolol组、atenolol组与ICI 118,551组LVSP和左心室±dp/dt_(max)较给药前降低,同时propranolol组与atenolol组RVSP和右心室±dp/dt_(max)较给药前明显降低(P0.05)。低氧通气5 min后,各组大鼠与常氧组相比动脉血氧分压(PaO_2)、LVSP和左心室±dp/dt_(max)均降低(P0.05);但右心室±dp/dt_(max)明显升高(P0.05);且低氧条件下control组心功能指标的变化程度均比propranolol组和atenolol组明显。结论:低氧应激时心脏β_1-AR的激活可能是心脏发挥代偿调节的重要方式,但右心室通过紧张源性扩张代偿表现出的右心舒缩功能增强对低氧下机体循环血流量的维持更为重要。     

Non-invasive assessment of cardiac function

Noninvasive assessment of cardiac function by Doppler echocardiography is reviewed. The heart propels the blood through the repeated sequence of systole and diastole. The systolic function is essential to maintain the biological function of the whole body. However, before the heart ejects the blood during systole, the heart must be filled up with blood during the preceding diastole. Thus, the diastolic function is as important as the systolic function. Although the diastolic function is traditionally assessed by hemodynamic parameters obtained in the cardiac catheterization laboratory, it has routinely been assessed by Doppler echocardiography in the echocardiographic laboratory in recent years. Since the concept of diastolic failure has widely spread, the important role of the transmitral flow in assessing the diastolic function has been well recognized. Besides the transmitral flow, the modalities for clinical assessment of the left ventricular diastolic function have been well developed. For example, the pulmonary venous flow has been easily obtained by a transthoracic approach, and the tissue Doppler technique provides important information about the diastolic function, and furthermore the color M-mode is applied for the flow propagation velocity of the left ventricular inflow. These modalities make it possible to assess the left ventricular diastolic function more precisely by Doppler echocardiography. Also, TEI index, strain rate and strain imaging, and wave intensity are mentioned.     

Temporary mechanical circulatory support for severe cardiac failure: experimental study

We describe a technique for mechanical cardiac assistance in an acute model of severe cardiac failure. Cardiac dysfunction was induced by a high dose of halothane in 13 dogs. Seven served as controls. Following median sternotomy, a pneumatically driven device was implanted in the other six dogs in a para-aortic position, using a simple surgical technique without cardiopulmonary bypass. The aorta was cross-clamped during cardiac assistance. During hemodynamic studies, the seven control animals with induced cardiac failure showed high end-diastolic left ventricular and right atrial pressures with low cardiac index and systolic left ventricular and aortic pressures. All dogs in this group died within 30 minutes. Use of a monovalvular cardiac assist device in the experimental group of six dogs to pump blood from the aortic root to the descending aorta in a counterpulsation manner, confirmed good preservation of systemic hemodynamic parameters after induction of heart failure. All animals in this treated group survived more than 45 minutes. Hemodynamically, the device acts as a new ventricle and the impaired left ventricle functionally becomes a left atrium. This condition is clinically appropriate for recovery of left ventricular function in severe acute myocardial failure.     

CardioClasp: a new passive device to reshape cardiac enlargement

In dilated heart failure, geometric distortions place an extra load on the myocardial cells. If this extra burden can be eliminated, the myocardial wall stress would decrease leading to improved systolic ventricular performance. In a dilated heart failure model, we wanted to see whether the CardioClasp (which uses two indenting bars to reshape the left ventricle [LV] as two widely communicating "lobes" of reduced radius) could improve systolic performance by passively reshaping the LV and reducing the wall stress. In mongrel dogs (n = 7; 25-27 kg), rapid ventricular pacing (210 ppm 1st week to 240 ppm 4th week) induced dilated heart failure. After 4 weeks, LV performance was evaluated at baseline and with the CardioClasp by measuring LV end-diastolic and peak LV systolic pressure, LV +dP/dt, LV -dP/ dt, and cardiac output. With the Clasp on, LV wall stress was reduced to 58.6+/-3.5 from 108.3+/-8.2 g/cm2. The fractional area of contraction (FAC) with the Clasp on (28.4+/-4.4) was significantly increased (p < 0.05) from baseline (20.8+/-4.6) and consistent with improved systolic performance. Cardiac output, LV peak systolic and end-diastolic pressures, and regional myocardial blood flow were unaltered. The Clasp was able to acutely reshape the left ventricle, while preserving the contractile mass, and reduced the tension on the myocardial cells and increased the fractional area of contraction without decreasing the systolic blood pressure.     

Mathematical model of cardiovascular mechanics for diagnostic analysis and treatment of heart failure: Part 1 model description and theoretical analysis

The planning of drug therapy for heart failure should involve both the diagnostic analysis of the patient’s defective state and a prediction of the drug effects on the identified state. We have devised a mathematical model of cardiovascular system mechanics, on which both quantitative diagnosis and evaluation of drug effects can be made. The model was composed of systemic and pulmonary circulatory networks including the dynamics of the left and right ventricles. The model of the ventricles can represent both systolic and diastolic problems in heart failure through the parameters of ventricular contractility and diastolic stiffness. Each vascular network was composed of arterial and venous resistances and total vascular capacitance. Patient’s ventricular and vascular parameters were estimated simultaneously from the clinically measurable haemodynamic variables based on the model. Despite the simplicity of the model, the results showed good agreement with clinical and experimental data. The clinically significant haemodynamic classification of heart failure by Forrester et al. (Forrester et al., 1977) was simulated well by the model. This model provides a useful basis for analysing pathophysiological states in heart failure and evaluating drug effects on the disease.     

Cardiomyocyte contractility and calcium handling partially recover after early deterioration during post‐infarction failure in rat

The aim of the study was to determine whether progression of heart failure is associated with deterioration of cardiomyocyte function. Cell dimensions, contractility and calcium transients were measured in cardiomyocytes isolated from the left ventricle of female Wistar rats 1, 4, and 13 weeks after coronary artery ligation or sham‐operation. Relative cardiomyocyte shortening decreased from 26% in controls to 11% 1 week after myocardial infarction and recovered to 18 and 20% after 4 and 13 weeks, respectively. Diastolic and systolic calcium concentrations increased markedly 1 week after myocardial infarction with subsequent reduction after 4 and 13 weeks. Time to 50% relaxation was prolonged by 31% after 1 week and 20% after 4 and 13 weeks with corresponding changes in diastolic calcium clearance. Cardiomyocyte length increased by 6, 24, and 26% after 1, 4 and 13 weeks, respectively, whereas myocyte width increased by 4, 11 and 27%. Cardiomyocytes adjacent to the infarct hypertrophied more and initially had more markedly impaired function than in the remote area. Left ventricular diastolic diameter assessed by echocardiography increased by 47, 66 and 84% after 1, 4 and 13 weeks, respectively, and systolic diameter increased by 120, 162 and 194%. Left ventricular end‐diastolic pressure increased from 6 mmHg to 24, 25 and 36 mmHg. Whereas initial deterioration of cardiac function is associated with reduced cardiomyocyte contractile function, chronic heart failure progression is not accompanied by further impairment of intrinsic cardiomyocyte contractility in this model. Cardiomyocyte hypertrophy and dysfunction are more marked adjacent to the infarction.     

Left ventricular heart failure model for testing cardiac assist devices

During the development of a new circulatory support system, we have used different animal models with and without heart failure for hemodynamic testing. As the normally functioning heart does not always allow for proper evaluation of a circulatory support system, a good and adjustable animal heart failure model is needed. The aim of the study was to develop a left ventricular failure model in calves for acute hemodynamic studies. The principle is based on the negative inotropic effect of drugs with bypass of the right ventricle. Seven calves were used in the study. Metoprolol and verapamil were both given intravenously as a bolus, and verapamil was continued as an infusion. The animals were equipped with a VVI pacemaker to treat the expected arteriovenous blockade. A centrifugal pump provided an adjustable flow with a two-stage inflow cannula draining both the upper and lower caval veins and with the outflow cannula in the pulmonary artery. The pump counteracted the effects of right ventricular failure and enabled us to increase the left atrial pressure to more than 20 mm Hg. Pressure in the left atrium rose from 5+/-3 to 25+/-4 mm Hg (p < 0.001), the left ventricular diastolic pressure increased from 2+/-3 to 17+/-7 mm Hg (p = 0.003), and the mean pulmonary pressure increased from 17+/-5 to 33+/-5 mm Hg (p < 0.001). Cardiac output was not significantly changed from 4.0+/-0.8 L/min in the healthy animals to 3.5+/-0.5 L/min (p = 0.25) in failure. The model allowed us to create an adjustable and isolated left ventricular failure well suited for short-term hemodynamic testing of a left ventricular support device.     

Atrial fibrillation and heart failure: Is atrial fibrillation a disease?

Atrial fibrillation in heart failure often occur together. The relationship between atrial fibrillation and heart failure has remained a subject of research. The main manifestation of the violation of hydrodynamics in heart failure is the increased end-diastolic pressure, which is transmitted through the intercommunicated system (left ventricle–left atrium–pulmonary veins–alveolar capillaries) causing increased pulmonary wedge pressure with the danger for pulmonary edema. End-diastolic pressure is the sum of left ventricle diastolic pressure and left atrial systolic pressure. Stopping the mechanical systole of the left atrium can reduce the pressure in the system in heart failure. Atrial fibrillation stops the mechanical systole of the left atrium and decreases the intercommunicating pressure and pulmonary wedge pressure. It is possible that atrial fibrillation is a mechanism for protection from increasing end-diastolic pressure and pulmonary wedge pressure, and prevents the danger of pulmonary edema. This hypothesis may explain the relationship between heart failure and atrial fibrillation and their frequent association.     

CHF患者血浆BNP检测的临床价值探讨

目的：探讨慢性心衰（CHF）患者血浆脑钠肽（BNP）检测的临床价值。方法：采用荧光免疫分析对341例CHF患者及55例健康对照者进行血浆BNP测定,同时以彩色多普勒超声心电动仪测定CHF患者左心室舒张末期内径（LVEDD）、左心室收缩末期内径（LVESD）、左心室射血分数（LVEF）,并与血浆BNP水平作相关性分析。结果：CHF组患者血浆BNP水平明显高于健康对照者（P〈0.01）,且不同心功能患者之间的血浆BNP含量亦存在显著差异（P〈0.01）;CHF组患者血浆BNP水平与LVEF、LVESD、LVEDD呈现良好的相关性（r分别为-0.62、＋0.54和＋0.60,P均〈0.01）。结论：BNP是评价CHF患者心室功能的灵敏指标。     

活血温阳益气中药复方对大鼠充血性心力衰竭的影响及机制研究

目的： 研究补气温阳、活血化瘀中药复方（组成：人参、黄芪、车前子、苏木、川芎、丹参、制附子、枳壳、桂枝）对大鼠充血性心力衰竭的影响机制。方法: 以大鼠腹腔注射盐酸阿霉素（ADR）制造充血性心衰动物模型,分为对照组、ADR心力衰竭模型组、心宝治疗组、活血温阳益气复方治疗组,并分别以生理盐水、心宝药液、活血温阳益气复方药液灌胃干预治疗,使用放免法、半定量逆转录-聚合酶链反应法（RT-PCR）及流式细胞技术测定心衰大鼠治疗前后血浆心钠素（ANP）、肾髓质精氨酸血管加压素依赖性水通道蛋白-2（AQP2）及热休克蛋白70（HSP70）的表达水平差异。结果: 活血温阳益气复方可显著提高心衰大鼠的心输出量、左室收缩内压,降低左心室舒张末压,改善左室内压最大变化速率,从而有效地改善了心衰大鼠的血流动力学;同时,该方能够显著降低心衰大鼠血浆ANP的水平和纠正心衰大鼠肾髓质AQP2蛋白的异常表达,并可提高白细胞中HSP70的转录和翻译水平。结论: 该活血温阳益气复方能有效减轻大鼠充血性心力衰竭的程度,其机制可能与其减少血浆ANP水平、矫正肾脏AQP2异常表达和增强 HSP70表达有关。     

Direct comparison of high‐temporal‐resolution CINE MRI with Doppler ultrasound for assessment of diastolic dysfunction in mice

Diastolic dysfunction is a sensitive early indicator of heart failure and can provide additional data to conventional measures of systolic function. Transmitral Doppler ultrasound, which measures the one‐dimensional flow of blood through the mitral valve, is currently the preferred method for the measurement of diastolic function, but the measurement of the left ventricular volume changes using high‐temporal‐resolution cinematic magnetic resonance imaging (CINE MRI) is an alternative approach which is emerging as a potentially more robust and user‐independent technique. Here, we investigated the performance of high‐temporal‐resolution CINE MRI and compared it with ultrasound for the detection of diastolic dysfunction in a mouse model of myocardial infarction. An in‐house, high‐temporal‐resolution, retrospectively gated CINE sequence was developed with a temporal resolution of 1 ms. Diastolic function in mice was assessed using a custom‐made, open‐source reconstruction package. Early (E) and late (A) left ventricular filling phases were easily identifiable, and these measurements were compared directly with high‐frequency, pulsed‐wave, Doppler ultrasound measurements of mitral valve inflow. A repeatability study established that high‐temporal‐resolution CINE MRI and Doppler ultrasound showed comparable accuracy when measuring E/A in normal control mice. However, when applied in a mouse model of myocardial infarction, high‐temporal‐resolution CINE MRI indicated diastolic heart failure (E/A = 0.94 ± 0.11), whereas ultrasound falsely detected normal cardiac function (E/A = 1.21 ± 0.11). The addition of high‐temporal‐resolution CINE MRI to preclinical imaging studies enhances the library of sequences available to cardiac researchers and potentially identifies diastolic heart failure early in disease progression.