Enlarged Left Ventricle Research Articles

Heterogeneous fate of perfusion and contraction after anterior wall acute myocardial infarction and effects on left ventricular remodeling

After acute myocardial infarction, patency of infarct vessel and extent of left venticular (LV) dysfunction are major determinants of ventricular remodeling. Spontaneous, delayed reperfusion in the infarct zone occurs in a sizeable number of patients well after the subacute phase. The aim of this study was to determine the relation between the occurrence of this spontaneous, delayed reperfusion and LV remodeling. In 84 patients, resting LV volumes, topography, regional function, and perfusion were quantitatively evaluated by 2-dimensional echocardiography and sestamibi tomography 5 weeks (study 1) and 7 months (study 2) after anterior Q-wave infarction. At study 2, LV end-diastolic volume increased by >15% in 17 patients (20%, LV remodeling); they had already had at study 1 significantly larger LV volumes, more severe hypoperfusion and wall motion abnormalities, and greater regional dilation than patients with stable LV volumes. Delayed reperfusion occurred in 8 of 17 patients with and in 42 of 67 patients without LV remodeling (47% vs 63%; p = NS). At study 2, LV regional dilation and end-diastolic volumes were stable in patients with, but increased in patients without, spontaneous reperfusion (from 25 ± 24% to 29 ± 26% at study 2 [p<0.05] and from 65 ± 14 to 68 ± 18 ml/m 2 [p <0.05]). At multivariate analysis, however, regional ventricular dilation at study 1 was the sole predictor of further LV remodeling. Thus, after acute myocardial infarction, spontaneous reperfusion occurring after 5 weeks plays only a minor role in influencing LV remodeling. Benefits from delayed reperfusion seem limited to patients with preserved LV volumes; patients with an enlarged left ventricle 5 weeks after acute infarction are prone to further LV remodeling, irrespective of delayed reperfusion.

Restoration of contractile function in the enlarged left ventricle by exclusion of remodeled akinetic anterior segment: surgical strategy, myocardial protection, and angiographic results.

A variant of the Dor cardioprotective approach for reducing ventricular volume was applied to 12 consecutive postinfarction patients with akinetic anterior segments. Cardioplegia was avoided for restoration, but used for revascularization and valve replacement. The continually perfused beating open heart was used for protection during surgical anterior ventricular restoration (SAVR). These ischemic cardiomyopathy patients (age 77 +/- 6 years) preoperatively had high LVEDVI (170 vs 75 mL/m2, normal) and LVESVI (132 vs 25 mL/m2, normal) and 20 +/- 8% ejection fraction (mean +/- S.D.). An oval patch with outer flange for hemostasis was used. Patients also underwent revascularization (10/12), reoperation (6/12), and valve procedures (6/12). Continuous perfusion of the beating open heart was used for cardiac protection during restoration. Blood cardioplegia was used for revascularization and valvular procedures. Transesophageal echocardiogram (TEE) estimated intraventricular contractility in all patients, and biplane ventriculograms were used in 8 patients to measure cardioreduction. Immediate hemodynamic performance was excellent in all patients, despite 178 +/- 34 minutes of bypass. Extracorporeal circulation was stopped 10 minutes after closing the ventriculotomy. No intraaortic balloon pump or LV assist devices were needed. Ejection fraction estimated by TEE increased from 20% to 45%; and biplane ventriculograms showed 28% reduction of LVEDVI, 39% reduction of LVESVI, and raised ejection fraction from 20% to 35%. The spherical ventricular shape after akinetic infarction was made into a more normal elliptical contour by this procedure. Subsequently, restoration may become as important as revascularization in treating akinetic segments after anterior infarction.

The outcome of peripartum cardiac failure in Zaria, Nigeria.

We have studied 227 women who had peripartum cardiac failure (PPCF) in Zaria, Nigeria, since 1969-72. This follow-up and review of survivors in 1993-95 depended chiefly on a Zaria woman (A. Abdullahi) and on her careful reporting. Overall, 31 (13.7%) were completely lost to follow-up, 17 (7.5%) were thought to be alive, and there were data on 179 others (78.8%). Of the 75 known deaths, 55 were cardiovascular--20 due to PPCF, 31 due to cardiac failure unrelated to pregnancy (CF), and four were due to a cerebrovascular accident. PPCF recurred in 13% of 551 subsequent pregnancies. Thirty-two women had a recurrence of PPCF only, and 27 an episode of CF only. Blood pressures rose steadily over the years. An enlarged left ventricle on discharge after the index admission predicted a poor prognosis. In 1993-5, we compared 100 survivors with 100 non-PPCF controls: 96 PPCF women but only 50 control women took extra salt (p = 0.0001). Significantly more PPCF women than controls had a diastolic pressure of 110 mm Hg (p = 0.011). The syndrome is probably provoked in potentially hypertensive women by the traditional practices of eating kanwa, which is rich in Na+, taking additional excess salt and heating the body after delivery. Evidence is presented that PPCF women are potentially hypertensive, and cannot handle the excess ingested sodium which therefore leads to hypervolaemia and thus PPCF.

Comparison of captopril and ibopamine in mild to moderate heart failure.

OBJECTIVE: To determine the effects of ibopamine 100 mg three times daily compared with captopril 25 mg three times daily on exercise capacity in patients with chronic heart failure. DESIGN:...

Expression of the Aryl Hydrocarbon Receptor (AhR) and AhR Nuclear Translocator during Chick Cardiogenesis Is Consistent with 2,3,7,8-Tetrachlorodibenzo-p-dioxin-Induced Heart Defects

We examined cardiotoxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the chick embryo and the cardiac expression of transcription factors, the aryl hydrocarbon receptor (AhR) which binds TCDD, and its dimer partner, the AhR nuclear translocator (Arnt). Chicken eggs were injected with control (triolein) or 1.0 pmol TCDD/g egg prior to incubation and collected on Day 10 when cardiomorphogenesis is complete. Relative to controls, TCDD increased heart wet weight (27.2 ± 0.5 versus 36.6 ± 1.3 mg,p< 0.001) and dry weight (2.7 ± 0.1 versus 3.1 ± 0.1 mg,p< 0.01), and tended to increase heart myosin content (3.5 ± 0.6 versus 6.3 ± 2.5 μg,p< 0.07), suggesting an increase in cardiac muscle mass and edema. Histologic and morphometric analyses revealed that 10/13 TCDD-exposed hearts exhibited enlarged right and left ventricles, thickened ventricular septum, and a thinner left ventricular wall with increased trabeculation, and 4/13 exhibited ventricular septal defects compared to controls (0/23). To evaluate AhR and Arnt expression, untreated chick embryos were collected on Days 2.2, 3, 4, 5, and 8 of incubation, preserved in Bouin's fixative, sectioned, and stained with AhR and Arnt antibodies. The AhR was expressed ubiquitously in cardiac myocytes, while Arnt expression was restricted to myocytes overlying developing septa: atrioventricular canal, outflow tract, and atrial and ventricular septa. Both proteins were absent from endocardium and endocardial-derived mesenchyme. In addition, cardiac expression of an AhR/Arnt target, cytochrome P4501A1, was restricted to myocardium coexpressing AhR and Arnt. Thus, the spatial and temporal expression of AhR and Arnt suggests that the developing myocardium and cardiac septa are potential targets of TCDD-induced teratogenicity, and such targets are also consistent with cardiac hypertrophy and septal defects observed following TCDD exposure.

Increased risk of coronary bypass surgery in left ventricular dysfunction with an enlarged left ventricle

Increased risk of coronary bypass surgery in left ventricular dysfunction with an enlarged left ventricle

Clinical and echocardiographic features of intermittent atrial fibrillation that predict recurrent atrial fibrillation

In addition to antithrombotic therapy, 2 treatment strategies for intermittent atrial fibrillation (AF) are evolving: suppression of AF or control of the ventricular response during AF. Clinical and echocardiographic features that predict recurrent AF may influence the choice of management. In this study, clinical, echocardiographic, and electrocardiograpnic data from 486 patients with intermittent AF enrolled in the Stroke Prevention in Atrial Fibrillation studies were analyzed. Patients with intermittent AF were younger (p < 0.001), had fewer incidences of systemic hypertension (p < 0.007) and heart failure (p < 0.001), and had more recent-onset AF than patients with constant AF. They also had a smaller mean left atrial diameter, a lower prevalence of a large (>5 cm) left atrium, better left ventricular performance by echo, and less mitral regurgitation. After a mean follow-up of 26 months, 51% of patients remained in sinus rhythm and 49% of patients developed recurrent AF, including 12% who had AF, as seen on all follow-up electrocardiograms. Clinical factors predicting recurrent AF were age, heart failure, and myocardial infarction. An enlarged left atrium was associated with recurrent intermittent AF; an enlarged left ventricle predicted conversion to constant AF. Thus, clinical and echocardiographic parameters predict recurrent AF in patients with intermittent nonvalvular AF.

Response of six patients with idiopathic hypereosinophilic syndrome to interferon alfa*

Response of six patients with idiopathic hypereosinophilic syndrome to interferon alfa*

Une cause inhabituelle d'épanchement péricardique au cours d'un drainage pleural

A 66-year-old man was admitted for mitral valve replacement required by a mitral regurgitation resulting in a severe heart failure. He also suffered from chronic respiratory failure, related to a left concavity cyphoscoliosis. Postoperatively, hypoxemia occurred. His chest X-ray showed a left pleural effusion indicating a percutaneous pleural drainage. A local anaesthesia with a 21 G needle was performed prior to drain insertion, which was easily introduced into the pleural cavity. A few minutes later, the patient experienced an acute haemorrhagic shock. He was immediately transferred into the operating room, where the cardiac surgeon discovered and treated a coronary artery effraction. The vascular lesion was attributed to the needle used for local anaesthesia. The patient was discharged twelve days later without sequelae. Two factors were responsible for this accident : the patient's cyphoscoliosis and his left ventricle enlargement. This complication is uncommon. However, in case of a particular patient's anatomy, it is suggested to use a score devised to anticipate the risk of a difficult pleural drainage. This score should include general, thoracic, spinal, cardiac, hepatic and splenic morphology.

Assessment of left ventricular enlargement from planar thallium-201 images

Although a subjective assessment of left ventricular (LV) size can be made from planar thallium images, the validity of this practice had not been critically assessed. The objective of this study was to determine the accuracy of planar thallium imaging in the assessment of LV size by using two-dimensional guided M-mode echocardiographic measurements as the standard. Consecutive patients ( n = 100) who had clinically indicated stress thallium and echocardiography done within a time interval of 1 month were selected. LV size was classified as dilated or normal on immediate and 4-hour-delayed thallium scans by the consensus of two blinded observers. When present, perfusion defects were noted. LV end-diastolic internal diameter (LVIDd) was measured on M-mode images. The mean LVIDd was 5.7 cm in patients with dilated LVs compared with 5.0 cm in those with normal LVs ( p < 0.01). By using an LVIDd of 5.6 cm as the upper limit of normal, the sensitivity and specificity of planar thallium imaging for detection of left ventricle enlargement were 87% and 86%, respectively. Corresponding positive and negative predictive accuracies in this population were 65% and 96%, respectively. There was a higher incidence of lixed defects in group 1 ( p < 0.01). We conclude that LV enlargement can be easily and reliably determined from routine planar thallium images.

Acetylcholine levels, choline acetyltransferase and acetylcholinesterase molecular forms during thyroxine-induced cardiac hypertrophy

The effects of left ventricular hypertrophy induced by hyperthyroidism on three biochemical markers of parasympathetic innervation were investigated. In response to subcutaneous injections of thyroxine (400 μg/kg: T 4) for 6 days, the left ventricle, but not the right, developed significant hypertrophy (20%). In the enlarged left ventricle, acetylcholine (ACh) content and choline acetyltransferase (ChAT) activity per chamber were elevated approx. 25–30%, although no change in these two markers was evident when the data were expressed per unit wet weight. Immunoblot analysis showed that the relative abundance of ChAT protein increased in the hypertrophied left ventricle in correlation with the increased ChAT activity. No changes in ACh content, ChAT activity and ChAT relative abundance were evident in the right ventricle of T 1-treated animals. Although hyperthyroidism did not alter AChE specific activity (per unit wet weight) in the left ventricle, the percent activities of the individual AChE globular forms were affected in this chamber. Specifically, T 4-treatment reduced the percent activity of globular (G) 4 AChE by 20% and increased that of the combined G 1 and G 2 AChE pool by 15%. Interestingly, in the hypertrophied left ventricle total AChE activity in its extracellular or functionally-relevant pool was reduced due to a loss of G 4 AChE activity. These results show that a compensatory increase in parasympathetic innervation can occur during hyperthyroid-induced left ventricular hypertrophy. However, the reduced activity of the functionally-relevant AChE pool suggests that the clearance of ACh after release may be slowed in the hypertrophied left ventricle.

The use of a somatostatin analog in the treatment of refractory hypotension after cardiopulmonary bypass

The patient was a 59-year-old male status post-prior mitral valve replacement (MVR) for mitral regurgitation (MR) and coronary artery bypass grafting (CABG) 6 months previously. He presented with recurrent MR due to endocarditis and a perivalvular leak, and was admitted with congestive heart failure (CHF) and shaking chills. Blood cultures were positive for Staphylococcus epidermidis. He had undergone 14 days of treatment with intravenous (IV) antibiotics, including vancomycin, gentamycin, and rifampin, which was associated with cessation of fevers and chills. His past medical history included hypertension, prior inferior myocardial infarction, and peripheral vascular disease. Additional medications included IV heparin, 1,000 u/h, and nitropaste, 2 inches every 6 hours. Laboratory values included a white blood cel1 count of 8,400 without bands, platelet count of 170,000/cc3, and a hematocrit of 29.7%. Cardiac catheterization revealed patent grafts, an enlarged left atrium (LA) and ventricle (LV), inferior and posterior hypokinesis, 3+ MR due to a perivalvular leak and a large LA vegetation. The patient was scheduled for a redo-MVR and debridement of his atrial vegetation. The patient was brought to the operating room where initial hemodynamics included a bloed pressure (BP) of 135165 mmHg, heart rate (HR) 65 beatsimin, centra1 venous pressure (CVP) 10 mmHg, pulmonary artery pressure (PAP) 43120 mmHg, pulmonary capillary wedge pressure (PCWP) 21 mmHg, with V waves to 38 mmHg, cardiac output (CO) of 5.0 Limin, systemic vascular resistance (SVR) of 1,200 dynes sec. cmes, and mixed venous oxygen saturation (SvOz) of 74%. Induction of anesthesia was carried out with 500 ug of sufentanil and 10 mg of pancuronium. After adequate relaxation, the trachea was intubated and mechanica1 ventilation was initiated with 100% oxygen. Maintenance of anesthesia was accomplished with sufentanil, pancuronium, and lorazepam (total sufentanil dose 1.5 mg, total lorazepam dose 4 mg). His antibiotics were continued in the operating room. The prebypass hemodynamics ranged from systolic bloed pressures (SBP) of 100-120 mmHg, HR 60-70 beatsimin, CVP 10-12 mmHg, PAP 35-40115-20 mmHg, CO 4-4.5 Limin, SVR of 1,300 dynes sec cmm5, and SvO2 68% to 80%.

Histologic evidence of myocardial damage in apparently healthy subjects with ventricular arrhythmias and myocardial dysfunction.

The association of ventricular arrhythmias and myocardial dysfunction could be considered an early step toward cardiomyopathy; therefore, we studied 28 patients in NYHA class I and II, characterized by complex ventricular arrhythmias (VA) on 24-h Holter monitoring and volumetric and/or contractile abnormalities on a standard two-dimensional echocardiogram (2-D echo). All patients underwent radioisotopic angiography, 20 patients complete hemodynamic study, and 15 patients endomyocardial biopsy. Ambulatory ECG monitoring showed the presence of frequent premature ventricular contractions in 14 patients (50%) and episodes of ventricular tachycardia in 16 patients (57%). 2-D echo showed mono- or biventricular enlargement and dyssynergies in 25 patients (89%) (left ventricle in 6, right ventricle in 11, both in 8). Two patients showed only left ventricle enlargement and one patient isolated left ventricular dyssynergies. Radioisotopic angiography showed mono- or biventricular ejection fraction reduction in 24 patients (85%) and regional dyssynergies in 24 patients (85%) in accordance with 2-D echo. Hemodynamic study showed in all patients normal coronary arteries, and right and left angiography confirmed enlargement and/or regional dyssynergies. Endomyocardial biopsy was abnormal in 11 of 15 patients: various degrees of hypertrophy, parcellar fibrosis, and adipogenic infiltration were found. Our preliminary data suggest that the simultaneous occurrence of ventricular arrhythmias and ventricular dyssynergies and/or enlargement in patients without apparent clinical heart disease may represent an early stage of dilated cardiomyopathy.

Early detection of left ventricular mural thrombi after acute Q wave myocardial infarction using 111In oxine-labelled autologous platelets

Autologous 111In oxine-labelled platelet scintigraphy was used to detect left ventricular thrombi in 20 patients with anterior and 18 patients with inferior Q wave myocardial infarction within 48-72 h. Left ventricular thrombi were found in 8/20 patients with anterior myocardial infarction and in 1/18 patients with inferior myocardial infarction, giving a total incidence of 24%. Patients with left ventricular thrombi were older (64.3 versus 58.2 years), had higher peak creatinine kinase (CK) levels (4523 versus 2749 IU 1-1), lower ejection fraction (19.5 versus 37.8%, P less than 0.005) and were more likely to have an enlarged left ventricle than those without left ventricular thrombi (87.5 versus 54.5%, P less than 0.001). Left ventricular thrombi were found overlying sites of myocardial infarction in 8 out of 9 patients. Apical left ventricular thrombi were 1.7 times more common than septal left ventricular thrombi. All patients received minidose heparin for prevention of deep venous thrombosis. This technique is complementary to echocardiography and may provide additional information in the difficult cases where the decision about full-dose anticoagulation is in doubt.

Dipole-tracing of abnormal slow brain potentials after cerebral stroke — EEG, PET, MRI correlations

A patient with major neurological deficits 5 years after a left cerebral infarction underwent correlative EEG, MRI and PET studies of cerebral blood flow and oxygen metabolism. The EEG showed abnormal slow electroencephalographic activity in the frontopolar region. The intracranial location of the slow electrical activity was estimated, as an equivalent current dipole, by using a newly developed dipole tracing (DT) method. The DT analysis showed that the dipole equivalent of the slow wave is approximately located at the frontal part of the left cingulate gyrus, away from the margins of the infarction and enlarged left lateral ventricle demonstrated by MRI, and in a region with intact oxygen consumption rate. The genesis of the slow wave is discussed.

Calcium antagonists as first-choice therapy for low-renin essential hypertension

A 55-year-old architect was referred to the Basel University Hypertension Clinic for evaluation of a 17-year history of high blood pressure in the range of 170—190/100—120 mm Hg. Antihypertensive treatment— including thiazide diuretics, beta blockers, alpha-methyldopa, and (early in the course) guanethidine and reserpine given alone or in combination—caused unwanted effects such as daytime fatigue, dry mouth, and impotence. The side effects interfered considerably with his quality of life. The family history was positive for hypertension. The patient had had 3 episodes of urinary tract infection but had no demonstrable abnormality by rapid-sequence intravenous pyelogram. He suffered often from pounding headaches, particularly during stress, but no palpitations, sweating, ororthostatic falls in blood pressure were observed. He had no additional cardiovascular risk factors: He had stopped smoking 7 years earlier, glucose tolerance was normal, and plasma cholesterol concentrations were below 6.5 mmol/liter. Body weight was 68 kg; height was 172 cm. Eight weeks following discontinuation of all antihypertensive medications, the blood pressure was 180/110 mm Hg with the patient seated. Physical examination showed evidence of an enlarged left ventricle, a grade li/Ill systolic ejection murmur, and a third heart sound. An electrocardiogram revealed left ventricular hypertrophy, and a plain chest film disclosed a cardiothoracic ratio of 0.6, the cardiac diameter being 15.5 cm. Laboratory evaluation revealed a serum potassium of 3.3

Use of the Left Infernal Thoracic Artery to Correct a Left Main Coronary Atresia

Dyspnea with a slightly enlarged heart was noticed in a five year old girl at a checkup. The cardiological investigation revealed an enlarged left ventricle with slight mitral regurgitation. The right coronary artery was enlarged and filled the entire left arterial system via collaterals. The left main coronary artery could not be detected. In addition, outflow of contrast medium into the large vessels was absent. With the diagnosis of left main coronary atresia, the left internal thoracic artery was implanted on to the proximal left anterior descendent in October 1985. In the control angiogram, the anastomosis conditions were normal, the left ventricle had decreased in size and contracted almost normally. The collaterals from the right could no longer be demonstrated. The child (now six years old) has full exercise tolerance today. In the ultrasonogram, the ventricle shows normal contraction behavior. Up to know, four cases with congenital main coronary atresia have been reported in the literature.

Digitalis: is it useful in congestive heart failure in patients in normal sinus rhythm?

The value of digoxin in the patient in normal sinus rhythm with chronic congestive heart failure continues to be controversial. Although many patients taking digoxin have no clinical deterioration after its discontinuance, there is a subgroup of patients (up to 30% of the total group) who demonstrate clinical deterioration on digoxin withdrawal. Patients with an S3 gallop and an enlarged left ventricle are especially likely to benefit from digoxin therapy. Furthermore, there is good evidence in patients with congestive heart failure that there is a persistent, chronic, positive inotropic effect with digoxin. Since digitalis is the only presently available, chronic, oral positive inotropic drug capable of increasing stroke volume at any given filling pressure, it should be used in patients with congestive heart failure.

Natural History of Dilated Cardiomyopathy

Seventy-seven patients with dilated cardiomyopathy (50 M and 27 F, aged 38 +/- 16 yrs) were followed up until Dec 31, 1985. Haemodynamic investigation was performed in all cases, and all pressure and left ventricular quantitative angiography parameters were collected. In no case did the coronary angiogram show significant lesions. Mean values of haemodynamic parameters for surviving and deceased patients were compared. Forty-six patients survived and 28 died during the follow-up period. Although all patients had an enlarged left ventricle and depressed contractility, survivors had either greater pressure/end systolic volume ratio or a greater stress/end systolic volume ratio. Survival curves confirm a particularly severe prognosis for patients with Suga index less than 1 or stress to end systolic volume ratio less than 2.5. Mass to volume ratio seems to affect two-year but not late survival. NYHA class does not indicate early survival. In conclusion, left ventricular function is obviously related to prognosis in these patients, but it seems still difficult to assess life expectancy from these parameters alone.

Postoperative regression of left ventricular dimensions in aortic insufficiency: A long-term echocardiographic study

The ability of preoperative M-mode echocardiography to predict the clinical course and the decrease in left ventricular size was assessed in 42 patients after uncomplicated valve replacement for isolated aortic insufficiency. During follow-up study, one patient died of chronic heart failure. The New York Heart Association functional class of the 41 survivors improved from 2.4 to 1.2. All patients had a preoperative M-mode echocardiogram. Serial echocardiographic measurements, available in 33 patients, showed a sustained decrease in left ventricular end-diastolic dimension after the first postoperative year from 73 +/- 8 to 57 +/- 9 mm at 6 to 12 months and to 53 +/- 9 mm at 3 years postoperatively (p less than 0.01). Left ventricular cross-sectional area decreased from 31 +/- 8 to 26 +/- 7 cm2 and then to 23 +/- 5 cm2 at the latest follow-up study (p less than 0.01). At 3 years postoperatively, M-mode echocardiograms were available in 37 patients: 24 had a normal left ventricular dimension (group 1), while 13 still had an enlarged left ventricle (group 2). The clinical course in these two groups was similar. The best preoperative predictor of persistent left ventricular enlargement was the end-diastolic dimension (p less than 0.05), whereas fractional shortening and the end-diastolic radius/thickness ratio were not predictive.(ABSTRACT TRUNCATED AT 250 WORDS)