Left Ventricular End-diastolic Size Research Articles

Modifiable risk factors of immediate and long-term outcomes in the operable and inoperable with left-sided infective endocarditis

ObjectivesTo evaluate the outcomes of left-sided infective endocarditis that can be operated on and cannot be operated on, and to focus on modifiable risk factors for immediate and long-term mortality. MethodsThis study retrospectively investigated patients with left-sided infective endocarditis who occurred in our medical center between January 2006 and November 2022. Results48 in-hospital deaths occurred (5.8 %, 48/832). We identified time from symptoms to admission and symptomatic neurological complications to be risk factors for multiple organ failure upon admission. Time from symptoms to admission and vegetation size in group of isolated medical treatment were significantly shorter than those in the group of heart operation. We also found that preoperative neurological complications, annulus destruction, levels of serum creatinine at 24 and 48 h post heart operation, and perivalvular leakage are risk factors for in-hospital mortality post heart operation. With 148 μmol/L as a cutoff level, the diagnostic sensitivity and specificity of serum creatinine level 48 h post surgery for in-hospital mortality post cardiac surgery are 100 % and 81.6 %, respectively. We found that vegetation size, ICU stay, postoperative serum creatinine at 48 h, left ventricular end diastolic size postoperative, and red blood cell transfusion were associated with all-time mortality. ConclusionsEarly diagnosis and treatment, improvement of surgical techniques, good protection for heart, kidney and blood and close follow-up are advocated to conduce to better immediate and long-term outcomes of the operable and inoperable with left-sided infective endocarditis.

The effectiveness of David procedure for aneurysm of the root and ascending part of the aorta

The aim – comparison of the results of David and Bentall operations in patients with aneurysms of the root and ascending aorta. Materials and methods. The one-centre study included 85 patients who underwent planned and urgent surgical treatment from 2019 to 2022. The patients were divided into two groups depending on the type of surgical intervention: the Bentall procedure was performed in the I group, while the David procedure was performed in the II group. Results. The study did not determine statistically significant differences in such indicators as the duration of artificial blood circulation and the time of aortic clamping. No significant differences were found in the duration of artificial lung ventilation and stay in the intensive care unit. However, the total length of hospital stay in the group of patients with David procedure was statistically lower and was 17.3 (8–35) days, while in the group with Bentall operation it was 23.7 (10–40) days (p = 0.01). The results of our analysis show that the early postoperative clinical results of the David and Bentall procedures are good and there are no significant differences. During David procedure, a statistically significant positive result of surgical treatment was revealed by such an indicator as the degree of insufficiency on the aortic valve (before and after the operation, 2.7 ± 1.3 and 0.8 ± 0.6, respectively, p < 0.05). In addition to the above indicator, significant results were found in the indicators: left ventricular end-diastolic size and left ventricular end-diastolic volume. Conclusions. The good immediate results of Bentall and David operations suggest that surgical repair of ascending and aortic root aneurysms using these operations can be equally safe when performed according to absolute anatomical indications and by an experienced surgical team. If both operations might be used in a particular patient, the valve-sparing operation should be preferred, given the lower risk of postoperative complications associated with the presence of a mechanical or biological prosthesis (such as thromboembolism, bleeding associated with anticoagulants, and structural deterioration of the bioprosthesis).

Фактори формування різних типів діастолічного наповнення лівого шлуночка в підлітків із патологією міокарда

Мета: вивчення головних компонентів формування порушеного діастолічного наповнення лівого шлуночка в підлітків із патологією міокарда. Матеріали та методи. Обстежено 110 підлітків із патологією міокарда віком 13–18 років, серед яких 40 — із порушенням ритму серця, 40 — із диспластичною кардіоміопатією, 30 — із первинною артеріальною гіпертензією. Морфофункціональні параметри серця вивчалися за допомогою ультразвукового дослідження за стандартною методикою. Функцію діастоли лівого шлуночка вивчали в імпульсному допплерівському режимі з картируванням трансмітрального потоку з верхівкового доступу чотирикамерного серця. Для адекватної оцінки діастолічної функції лівого шлуночка і визначення найбільш ранніх її порушень підліткам проводилася проба з ізометричним навантаженням. На підставі отриманих результатів підлітки були розподілені за показником співвідношення Е/А. З метою виявлення прихованих загальних факторів, що пояснюють зв’язок між показниками, було застосовано факторний аналіз, а саме метод головних компонент. Усі статистичні процедури проводили з використанням пакетів прикладних програм Statgrafics Centurion. Результати. На початкових етапах становлення діастолічної дисфункції міокарда лівого шлуночка серця в підлітків значну роль відіграє низка факторів, що можна умовно позначити як геометричний, функціональний та нейрогуморальний фактори, які включаються послідовно в патологічний процес. Так, при формуванні 1-го типу діастолічної дисфункції лівого шлуночка на першому місці знаходиться нейрогуморальний фактор, а саме активація симпатоадреналової системи, далі в патологічний процес залучається периферичний судинний тонус та, як наслідок, геометричний фактор — зміна розмірів лівого передсердя. При формуванні 2-го типу діастолічної дисфункції лівого шлуночка в процес послідовно залучається ренін-ангіотензинова система, а саме ренін, функціональний фактор представлено показниками загального периферичного судинного опору та хвилинного об’єму, а геометричний складається з діаметра лівого передсердя та кінцево-діастолічного розміру лівого шлуночка. Формування 3-го типу діастолічної дисфункції лівого шлуночка відбувається під впливом таких складових нейрогуморальної системи, як ренін та ангіотензин II, потім послідовно в процес залучаються периферичний судинний тонус та геометричний фактор у вигляді показників діаметра лівого передсердя та кінцево-діастолічного розміру лівого шлуночка. Отже, на початкових етапах становлення діастолічної дисфункції лівого шлуночка в підлітків із патологією міокарда значну роль відіграють симпатоадреналова система, периферичний судинний тонус та функція лівого передсердя, а далі послідовно підключається ренін-ангіотензинова система, що викликає підвищення жорсткості міокарда та, як наслідок, включення в патологічний процес не тільки лівого передсердя, але й структури (кінцево-діастолічний об’єм) і функції лівого шлуночка серця (ударний об’єм).

RELATIONS OF THE AORTIC STIFFNESS AND CENTRAL BLOOD PRESSURE WITH FEATURES OF THE LEFT VENTRICLE IN ASCENDING AORTIC ANEURYSM

Objective: To reveal relations of the arterial stiffness, central blood pressure (BP) with left ventricular (LV) structure and function in patients with ascending aortic aneurysms (AAA). Design and method: We examined 44 patients with AAA (30 (68%) males; 55 ± 13 years old) before AAA surgical repair. Office brachial BP (BBP) was measured by OMRON (Japan). Arterial stiffness was evaluated by carotid-femoral pulse wave velocity (PWV). Central BP (CBP) and PWV were measured with the SphygmoCor (Australia). Ambulatory BP monitoring was performed with the BPLab (Russia) with 24-hour measuring of BBP and CBP. A transthoracic echocardiographic examination was performed with a Vivid 7 GE (USA). Results: Hypertension was observed in 40 (91%) patients. LV hypertrophy (LVH) was found in 41 (94%) patients (mean LV mass index (LVMI) 163 ± 48 g/m2). Diastolic dysfunction presented in 39 (89%) patients. PWV was inversely related to the AAA diameter (r = - 0.389, P = 0.03): PWV decreased with an increase of the aortic diameter at the level of the aortic root. A decrease of PWV correlated with a decline of relative wall thickness (RWT) (r = 0.365, P = 0.040), but eccentric LVH occurred only in 17 (38%) patients with AAA. PWV correlated directly with LV ejection fraction (r = 0.464, P = 0.048), but PWV was inversely related to LV end-diastolic size (LVED) (r = -0.533, P = 0.003). Rigid type diastolic disturbances (E/A ratio>2) were negatively correlated with PWV (r = -0.652, P = 0.041). Office pulse BBP and CBP correlated with the LVMI (r = 0.428, P = 0.019 and r = 0.508, P = 0.002, respectively). 24-hour pulse BBP and CBP were correlated with LVMI (r = 0.660, P = 0.018 and r = 0.721, P = 0.008, respectively). The increase of LVED had a closer association with office pulse CBP (r = 0.459, P = 0.007) than with office pulse BBP (r = 0.410, P = 0.017). Conclusions: Eccentric LV hypertrophy was accompanied by a significant reduction of PWV in patients with AAA. The severity of the diastolic dysfunction increased with a decline of PWV. PWV is probably not suitable for accurate assessment of the arterial stiffness in AAA due to the apparent confounding effect of aortic diameter. In AAA central pulse BP had a closer association with LVMI and LVED than brachial pulse BP.

Unveiling the Mystery of Peripartum Cardiomyopathy: A Traditional Review.

Peripartum cardiomyopathy (PPCM) can be classified as a variant of dilated cardiomyopathy identified usually within the first five months of delivery or during the last month of pregnancy. This condition presents as systolic heart failure. PPCM affects thousands of women in the United States each year. Even though it was first noticed in the 1800s, its etiology remains unknown. This study aims to review the pathophysiology and management of PPCM and explore the possible outcomes of peripartum cardiomyopathy. PPCM can lead to maternal death if diagnosis or treatment is delayed. Diagnosing PPCM has been challenging because it can be misdiagnosed or perceived as a sign of pregnancy since most of the symptoms of PPCM strongly match those within the typical pregnancy continuum and postpartum cycle. Patients' implications are fatal and carry a high mortality rate when PPCM is misdiagnosed or treatment is delayed. To accurately identify PPCM, using echocardiography, the left ventricular end-diastolic size and the ejection fraction should be measured to determine the severity of PPCM. Managing peripartum cardiomyopathy involves using traditional treatments for heart failure. Therapeutic recommendations are made depending on the patient's status (pregnancy, breastfeeding, postpartum) while considering the drug-safety profiles before administration. Some other treatments have also been used to control PPCM depending on how severe it has become; for example, antiarrhythmics have been used to treat cardiac arrhythmias when they ensue. In extreme cases, mechanical assistance and transplantation could be required. Based on the proposed pathophysiology involving the 16kDA anti-angiogenic sub-fragment, bromocriptine may be used even though it still needs more assessment due to limited evidence.Using PubMed as a major search resource, a thorough analysis of publications was carried out after incorporating this review's inclusion and exclusion criteria. A total of 455,141 publications were found using keywords and keyword combinations. With a careful selection of articles, 31 publications provided relevant information on our primary endpoint. All articles in this examination were chosen without limitation to the type of study, including clinical trials, review articles, meta-analyses, and so on. Our review suggests that, based on factors such as early detection and management, disease severity, ethnicity, and quality of patient care, patients with PPCM presented different outcomes and prognosis. However, despite PPCM's high mortality rate and its risk of recurrence, most patients tend to recover within six months of disease onset.

ПРОГНОЗУВАННЯ РОЗВИТКУ ХРОНІЧНОЇ ІШЕМІЧНОЇ(ВІНЦЕВОЇ) ХВОРОБИ СЕРЦЯ У ПАЦІЄНТІВ З МЕТАБОЛІЧНИМ СИНДРОМОМ ПРИ ОЖИРІННІ З ВРАХУВАННЯМ ВІКОВИХ ТА ГЕНДЕРНИХ ОСОБЛИВОСТЕЙ

Diagnostic criteria of chronic coronary artery disease (CAD) with metabolic syndrome (MS) in case of obesity were singled out in the research. Gender and age were considered as well.Material and methods. 138 patients with MS and II – IIІ degree obesity with a preliminary diagnosis of CAD were examined. The first group was represented by individuals aged 28-40, the second group was represented by patients aged 40-70. The third group was represented by 30-40-year old female patients and the fourth group – by 40-70-year-old female patients. Levels of prolactin, cortisol, free thyroxine (fT4), thyroid-stimulating hormone (TSH), lipid spectrum, were determined for all patients. Ultrasonography of the heart was also taken into account.According to the results of the study of lipid metabolism, increase of low-density lipoprotein cholesterol (LDL CH), triglycerides (TG), very low-density lipoprotein cholesterol (VLDL CH), total cholesterol (TCH), coefficient of atherosclerosis (CA) and decrease of high-density lipoprotein cholesterol (HDL CH) were observed in patients of 1, 2 and 4 groups.Results. Left ventricular posterior wall thickness (LVPWT), interventricular septal thickness (IVST), left ventricular end-diastolic size (LVEDS) and left atrium anteroposterior dimension (LA) were enlarged in patients of 1, 2 and 4 groups (diagnosis of chronic CAD was confirmed) according to results of echocardiography.According to the results of lipid spectrum study, high levels of TG and VLDL were observed in patients of the 3rd group (diagnosis of chronic CAD was not confirmed).According to ultrasonography results, increased IVST and LA dilatation indicated the development of metabolic cardiopathy in patients of this group.Increased levels of prolactin, cortisol, and TSH were observed in patients of group 3. An increased of level of TSH was observed in the second and fourth groups, unlike the first group, where the level of TSH was normal.Prolactin level was within normal limits in groups 1, 2, 4. High levels of TSH and normal levels of cortisol were recorded in groups 2 and 4, in contrast to group 1, which had a normal TSH level and increased cortisol level.Gender differences in the first and third group: increased TSH and prolactin levels for women of the 3rd group and normal levels of these hormones for men of the 1st group. Increased levels of TSH with normal content of prolactin were observed in the second and fourth groups.Conclusions. During the estimation of research results, it may be stated that the increased prolactin level in group 3 concurs clinically with the absence of CAD and can serve as a diagnostic marker of this condition.

Двойная блокада рецепторов альдостерона как способ устранения негативного воздействия нестероидных противовоспалительных препаратов при хронической сердечной недостаточности

Loop diuretic (such as torasemide) can be recommended for elimination of negative consequences of the use of nonsteroidal anti-inflammatory drugs in patients with chronic heart failure.

Efficiency of immunosuppressive therapy in virus-negative and virus-positive patients with morphologically verified lymphocytic myocarditis

To evaluate the efficiency of immunosuppressive therapy (IST) in virus-negative (V-) and virus-positive (V+) patients with lymphocytic myocarditis (LM). 60 patients (45 males) (mean age 46.7±11.8 years) with dilated cardiomyopathy (mean left ventricular (LV) end diastolic size (EDS) 6.7±0.7 cm; ejection fraction (EF) 26.2±9.1%) were examined. The diagnosis of active/borderline LM was verified by right ventricular endomyocardial biopsy in 38 patients, by intraoperative LV biopsy in 10, in the study of explanted hearts from 3 patients and at autopsy in 9. The investigators determined the genomes of parvovirus B19, herpes viruses types 1, 2 and 6, Epstein-Barr (EBV), zoster, and cytomegalovirus in the blood and myocardium and, if antibodies were present in the blood, hepatitis B and C viruses, as well as antibodies against antigens in the endothelium, cardiomyocytes and their nuclei, smooth muscles, fibers of the conducting system. IST was used in terms of histological, immune, and viral activities. IST was performed in 22 V+ patients (Group 1) and in 24 V- patients (Group 2); this was not done in 10 V+ patients (Group 3) and V- patients (Group 4). IST comprised methylprednisolone at a mean dose of 24 mg/day (n=40), hydroxychloroquine 200 mg/day (n=20), azathioprine at a mean dose of 150 mg/day (n=21); antiviral therapy included acyclovir, ganciclovir, intravenous immunoglobulin (n=24). The follow-up period was 19 (7.3-40.3) months. The viral genome was detected in the myocardium of 32 patients who made up a V+ group. The degree of histological activity did not differ in relation to the presence of viral genome in the myocardium. The degree of immune activity (anticardiolipin antibody titers) in the V+ patients was as high as that in V- ones. At baseline, the V+ patients had a significantly higher LV EDS and a lower EF than the V- patients. Overall, IST only could lead to a significant increase in EF (from 26.5±0.9 to 36.0±10.8%; p<0.001) and reductions in NYHA functional class from III to II (p<0.001), LV EDS (from 6.7±0.7 to 6.4±0.8 cm; p<0.01), pulmonary artery systolic pressure (from 48.9±15.5 to 39.4±11.5 mm Hg (p<0.01); the IST group had significantly lower mortality rates than the non-IST group (23.9 and 64.3%; p<0.01). At the same time, a significant trend was seen in both V- and V+ patients. The mortality rate in the V+ patients, as a whole, was higher (46.9 and 17.9%; p<0.05). IST leads to a significant improvement of functional indices and it is associated with lower mortality rates in both myocardial V- and V+ patients with LM. A more than 10% EF increase in the first 2 months is associated with a good prognosis. The presence of viral genome in the myocardium (primarily herpesviruses rather than parvovirus-19) is accompanied by more severe initial dysfunction, a less pronounced effect of IST, and higher mortality rates. However, the positive effect of IST also persists in V+ patients. No positive changes (a decrease in EF was observed) were absent only in IST-naïve V+ patients.

Диференційно-діаґностичні особливості метаболічного синдрому з ожирінням при наявності та відсутності хронічної ішемічної хвороби серця з врахуванням статі

Aim.&nbsp;The differences between metabolic syndrome (MS) with obesity with or without comorbid pathology (chronic coronary artery disease i.e. CAD) were explicated in the research. Material and Methods.&nbsp;126 patients with MS were examined. MS without chronic CAD was diagnosed in 82 patients and MS with chronic CAD was diagnosed in 44 patients. Levels of lipid spectrum, cortisol, prolactin, thyroid-stimulating hormone (TSH), free thyroxinе (fT4), glycosylated hemoglobin (HbAlc), and glucose were determined in all patients. Ultrasonography of the heart was taken into account. Results and Discussion.&nbsp;Increased levels of cortisol, TSH and prolactin (only in women) were observed in patients with MS without chronic CAD. Normal levels of cortisol and prolactin were observed in the patients with MS and chronic CAD simultaneously with increase of TSH levels in men and women the fT4 level was within normal limits. Changes in given parameters were accompanied by increase in total cholesterol (TCH), triglycerides (TG), low-density lipoprotein cholesterol (LDL CH) and very low-density lipoprotein cholesterol (VLDL CH) and decrease in high-density lipoprotein cholesterol (HDL CH) in patients with MS and chronic CAD regardless of gender, whereas only TG and VLDL CH were increased in patients with MS with obesity without chronic CAD. Interventricular septal thickness(IVST), left ventricular posterior wall thickness (LVPWT), left ventricular end-diastolic size (LVEDS) as well as left atrium anteroposterior dimension (LA) increased in men and women with comorbid pathology, whereas only IVST and LA were increased in MS. Increased prolactin and TSH in women in contrast to men in MS with obesity have been established. High levels of TSH were recorded in the presence of combined pathology regardless of gender.&nbsp; Conclusion.&nbsp;Thus, diagnostic features of MS with obesity without chronic CAD are characterized by hormonal abnormalities in women, in contrast to men, whereas endocrine changes are not gender-specific in the presence of comorbid pathology.

The Impact of Asymptomatic Left Ventricular Dilatation on the Course of Anterior Myocardial Infarction.

to elucidate effect of asymptomatic left ventricular (LV) dilatation on the course of myocardial infarction (MI). LV remodeling and diastolic function, as well as inter- and intraventricular asynchrony were studied in 58 patients with primary anterior MI without signs of heart failure and ejection fraction >40% on month 12 of the disease. Patients were divided into 2 groups: with normal-sized left ventricle (LV end diastolic size [EDS] <5.5 cm) (n=28), and with mild LV dilatation (LV EDS 5.6-5.9 cm) (n=30). At month 12 of MI patients with asymptomatic LV dilatation were characterized by more pronounced signs of pathological remodeling, diastolic LV dysfunction, inter- and intraventricular asynchrony.

Sex-Specific Normalized Reference Values of Heart and Great Vessel Dimensions in Cardiac CT Angiography

Published cardiac CT angiography (CTA) reference measurements for the cardiac chambers, aorta, and pulmonary artery (PA) are incomplete and compromised by study population, coronary artery disease (CAD), or its risk factors. The purpose of our study was to establish sex-specific normalized ranges of cardiac chamber size, wall thickness, ejection fraction (EF), and aorta and PA diameter on cardiac CTA in a population without CAD or its risk factors. Seventy-six patients (38 men and 38 women) without known diabetes; hypertension; smoking history; or evidence of structural heart, vascular, or coronary artery diseases underwent 64-MDCTA. Obtained left atrial (LA) size, left ventricular (LV) volumes, LV wall thickness, thoracic aorta, and PA diameter measurements were normalized to body surface area (BSA). There were statistically significant differences noted between men and women for all measured left-sided heart and great vessel measurements. After normalization to BSA, only chamber dimensions and ascending aorta and left PA sizes remained significantly different. Selected normalized measurements for men versus women, respectively, include LA area, 10.6 ± 2.1 versus 12.3 ± 2.1 cm²/m²; LV end-diastolic size, 72.4 ± 15.1 versus 60.9 ± 13.3 mL/m²; EF, 67% ± 7% versus 72% ± 8%; aortic sinus, 1.6 ± 0.2 versus 1.7 ± 0.2 cm/m²; ascending aorta, 1.4 ± 0.2 versus 1.6 ± 0.2 cm/m²; descending aorta, 1.1 ± 0.1 versus 1.2 ± 0.1 cm/m²; main PA, 1.3 ± 0.1 versus 1.4 ± 0.1 cm/m²; right PA, 1.1 ± 0.1 versus 1.1 ± 0.2 cm/m²; and left PA, 1.0 ± 0.1 versus 1.1 ± 0.1 cm/m². Cardiac CTA measurements of the left cardiac chambers, thoracic aorta, and pulmonary arteries were established for a population without CAD or its risk factors.

Time course of left ventricular volumes in severe congestive heart failure patients treated by optimized AV sequential left ventricular pacing alone—A 3-dimensional echocardiographic study

This study evaluates the acute and chronic resynchronizing effects of AV sequential left ventricular (LV) pacing on LV function in patients with impaired cardiac function and conduction disorders by 3-dimensional transesophageal echocardiography. Twenty-nine patients with congestive heart failure, with LV ejection fraction (LVEF) < or = 30%, QRS duration > or = 120 milliseconds, and New York Heart Association Class II to IV, were implanted with a cardiac resynchronization device using an LV lead only, according to the invasively determined hemodynamic optimal pacing site and AV delay. Patients underwent 3-dimensional transesophageal echocardiography before randomization to treatment (baseline) and at 12-month follow-up (resynchronization--12 months). Three-dimensional volumes were acquired on resynchronization and during intermittent switch-off at intrinsic depolarization. The values of stroke volume were 43.2 +/- 13.3 (intrinsic-baseline), 51.7 +/- 17.4 (intrinsic--12 months), 57.2 +/- 15.6 (resynchronization-baseline), and 64.6 +/- 18.9 (resynchronization--12 months). Analysis of variance demonstrated a significant effect of resynchronization at different periods (P < .001) and a significant time effect (P < .05) for stroke volume. Similar results were observed with ejection fraction (LVEF). No effect was observed with LV end-diastolic volume, whereas a therapy effect with no time effect was observed with LV end-systolic volume. A significant acute increase of LV stroke volume and LVEF was found by resynchronization by LV pacing alone. A continuous improvement of LV stroke volume and LVEF occurred with time of follow-up (reverse remodeling). The initial therapeutic effect persisted during 12-month follow-up independently of time of follow-up and QRS width. No significant decrease of LV end-diastolic size during chronic resynchronization was detected in contrast to previous studies with resynchronization by biventricular pacing.

Reverse remodeling in heart failure with intensification of vasodilator therapy.

Heart failure therapy with beta-receptor blockade has been shown to effect a partial reversal of left ventricular (LV) remodeling in heart failure. We tested the hypothesis that, in the absence of beta blockade, uptitration of angiotensin-converting enzyme (ACE) inhibitor and nitrate therapy over conventional dosages would improve symptoms as well as LV function in patients with severe heart failure. For patients with nonischemic or ischemic cardiomyopathy, intensive high-dose angiotensin-converting enzyme inhibitor and nitrate therapy was uptitrated. Echocardiograms were obtained semiannually and evaluated in a blinded fashion. Of 99 patients in the study, aged 55 +/- 13 years, with heart failure for 5.2 +/- 3.1 years, 74 were men, 69 were Caucasian, and 34 had ischemic cardiomyopathy. The final dosage of enalapril was 40 +/- 23 mg/day of isosorbide dinitrate it was 153 +/- 127 mg/day. Initial New York Heart Association classification improved from 2.8 +/- 0.9 to 1.7 +/- 0.9 (p < 0.001) in 2.7 years of follow-up. Of the 99 patients, 72 further improved their ejection fraction. For the whole group, ejection fraction increased from 21 +/- 9% to 30 +/- 13% in 6 months (p < 0.001), with a reduction in LV end-diastolic size from 6.6 +/- 0.9 to 6.3 +/- 1.0 cm (p = 0.002), a decrease in the severity of mitral regurgitation from mild/moderate to only mild. Resting heart rate declined with no change over time in systemic systolic blood pressure. Final ejection fraction for nonischemic patients (n = 65) was 36 +/- 16% versus 23 +/- 9% for the ischemic population. Uptitration of high-dose ACE inhibitor and nitrate therapy to higher doses is well tolerated in severe heart failure, further improves both clinical status and LV systolic function, and is more effective in nonischemic than in ischemic cardiomyopathy.

Pulmonary injury depresses cardiac systolic function through Starling mechanism.

To determine whether pulmonary microvascular injury or lung hyperinflation changes left ventricular (LV) performance and whether ventricular interaction plays a role in mediating such changes, we studied seven open-chest, closed-pericardium, anesthetized dogs before and after right ventricular (RV) injections of 150- to 200-micron glass beads. Because people with pulmonary disease are often treated with positive end-expiratory pressure, we also hyperinflated the lungs before and after creating the pulmonary microvascular injury. Measurements of LV and RV pressures and dimensions were taken at end expiration during the basal state, during lung hyperinflation, and after microvascular injury at RV end-diastolic pressures of 5, 10, and 15 mmHg produced by volume loading. Acute volume loading produced upward shifts in the LV diastolic pressure-size curve both before and after microvascular injury. Neither microvascular injury nor lung hyperinflation substantially affected the LV diastolic pressure-size relationship. LV end-diastolic size determined LV stroke work with no consistent independent influence of microvascular injury or lung hyperinflation. Neither microvascular injury nor lung hyperinflation depressed systolic performance beyond that associated with changes in end-diastolic heart size.

The influence of heart rate on echocardiographic assessment of aerobic training.

AbstractThe purpose of this investigation was to determine if echocardiographic measures of ventricular structure and function ascribed to aerobic training might be an artifact of heart rate (HR) differences between trained and untrained subjects. Comparisons were made at rest, of 10 young, male, aerobically well‐trained athletes [((VO2)max 65&gt;ml/kg/min] and 10 young, healthy controls [((VO2)max&lt;56ml/kg/min]. Additionally, the echocardiographic responses to low (HR=80 beats/min) and moderate intensity (HR=120 beats/min) supine cycling exercise were analyzed. Echocardiographic measures were made as described by Sahnet al. (1978). Results of echocardiographic comparisons between groups, both during supine rest and at a constant heart rate of 80 beats/min during supine cycling confirmed that athletes had significantly greater left ventricular mass (LV mass) and end‐diastolic size per square meter of body surface area (p&lt;0.05). When supine cycling loads were increased to elevate HR to 120 beats/min in groups of 7 athletes and 5 controls, athletes exhibited a progressive and significant (p&lt;0.05) enlargement of left ventricular end‐diastolic size (LVEDS), while left ventricular end‐systolic size (LVESS) showed negligible change. The control group showed little change in LVEDS, but decreased LVESS significantly (p&lt;0.05). Contractility measures, i.e., estimated ejection fraction (EF) and velocity of circumferential shortening ( (Vcf) increased in both groups in a similar manner. It was concluded that echocardiographic differences in ventricular structure and function observed between aerobically trained and untrained subjects are not an artifact of heart rate differences. Clearly, aerobic training results in increased LV mass and diastolic size which allows for further dilitation with supine exercise. Aerobic training does not appear to alter indices of myocardial contractility.

Effects of acute increases in left ventricular preload on indices of myocardial function in conscious, unrestrained and intact, tranquilized baboons.

The effects of acute volume loading were examined on indices of left ventricular (LV) function in conscious, unrestrained and intact, tranquilized baboons. Experiments were conducted 1-3 mo after implantation of ultrasonic transducers to measure LV internal diameter and wall thickness, and miniature LV pressure gauges and aortic and left atrial catheters. In 10 intact, tranquilized baboons, rapid volume loading with saline increased LV end-diastolic pressure by 23.7+/-2.6 mm Hg, LV end-diastolic diameter by 7.8+/-1.5%, LV stroke work by 37.5+/-7.8%, while mean arterial pressure and peak LV wall stress did not change significantly. Despite the increase in preload and activation of the Frank-Starling mechanism, LV dP/dt(max) and the maximum velocity of myocardial fiber shortening (LV dD/dt(max)) did not change. Volume loading after beta-adrenergic or combined beta-adrenergic and cholinergic blockades or volume loading with blood instead of saline also failed to augment LV dP/dt(max) and LV dD/dt(max) despite the increase in preload. In order to volume load the baboons in the conscious state, a radiofrequency (RF) interrogator system was devised, which upon receipt of a radio command, activated a battery operated pump to infuse 1,000 ml of saline i.v. to the baboons. In these experiments, preload rose, i.e., LV end-diastolic diameter increased by 13.9+/-2.1% and the Frank-Starling mechanism could be demonstrated, i.e., stroke work rose by 42.8+/-7.4%, but LV dP/dt(max) and LV dD/dt(max) did not change. After preload was depressed by hemorrhage, the rapid infusion of either blood or saline increased LV dP/dt(max) by 92.7+/-18.5% and LV dD/dt(max) by 64.3+/-10.1%. Thus, acute volume loading in the conscious baboons increased LV end-diastolic size and even stroke work substantially. However, preload dependency of LV dP/dt(max) and the maximum velocity of myocardial fiber shortening was only encountered at low levels of LV preload.