Takotsubo-like left ventricular dysfunction with delayed recovery of left ventricular shape: a case report

A 70-year-old woman was admitted to our hospital because of left ventricular dysfunction, which was observed after permanent pacemaker implantation in another hospital. The left ventricular dysfunction was apical ballooning. Left ventriculography demonstrated takotsubo-like shape. However, the dysfunction did not improve immediately with medical treatment. In this case, 75% stenosis was observed in the left anterior descending artery. We suppose that this lesion corresponded to the delayed recovery of the dysfunction and performed coronary intervention. The takotsubo-like shape improved gradually for about 1 year. Whether the coronary intervention was effective for the recovery of the dysfunction is unclear, this clinical course was interesting in evaluating the delayed recovery of takotsubo-like left ventricular dysfunction.     

Stroke and ventricular dysfunction in a patient with isolated left ventricular noncompaction

A 44-year-old woman developed a cardioembolic stroke. Transthoracic echocardiography demonstrated isolated noncompaction of the ventricular myocardium. Left ventricular systolic function was mildly depressed, which severely decreased during 3 months after discharge. The embolic stroke might occur when the ventricular systolic function had begun to deteriorate. The proper time to start anticoagulation in isolated noncompaction of ventricular myocardium patients may be when left ventricular systolic function decreases below normal.     

Regional left ventricular dysfunction in a patient with severe prolonged anemia

A 47-year-old woman with severe prolonged anemia developed heart failure. After treatment of the heart failure and anemia, she showed regional dysfunction of the left ventricular wall and myocardial fatty acid metabolism was disturbed in these sites. Coronary arteriography showed normal images. It took about 4 months to recover both left ventricular wall motion and fatty acid metabolism. Prolonged decrease of oxygen supply to the myocardium, which is caused by severe prolonged anemia, seemed to affect the myocardial function in this case, which could be another model of anemia-related myocardial dysfunction.     

Managing the post-myocardial infarction patient with asymptomatic left ventricular dysfunction

The percentage of post-myocardial infarction (MI) patients with asymptomatic left ventricular dysfunction (ALVD) is now estimated at 10%, and that number is expected to grow as reperfusion procedures increasingly become routine. Since average all-cause mortality risk in these patients is high (up to 27%), definitive diagnostics are recommended to screen all post-MI patients for ALVD, defined as left ventricular systolic dysfunction in the absence of heart failure symptoms. Post-MI management strategies for patients with ALVD target the two routes of progression to heart failure: (1) cardiac remodeling mediated by neurohormonal activation, and (2) continued and recurrent myocardial ischemic events. Clinical trials of neurohormonal antagonists in post-MI ALVD patients have shown that angiotensin-converting enzyme inhibitors attenuate left ventircular remodeling and that beta-blocker therapy reverses remodeling for patients already on angiotensin-converting enzyme inhibitor therapy. Neurohormonal antagonist therapy is also associated with significant reductions in sudden death in post-MI ALVD patients.     

Isolated left ventricular diverticulum in an asymptomatic patient

A 47-year-old male with intermediate risk of coronary arterydisease and atypical chest pain was referred to our hospitalfor multislice computed tomography (MSCT) coronary     

Reversible left ventricular dysfunction

The extent and degree of myocardial viability are important parameters in the risk stratification of patients with significant left ventricular dysfunction secondary to coronary artery disease. Although several imaging modalities can identify viable myocardium, dobutamine stress echocardiography has gained considerable importance as an accurate, safe, and reliable method. In patients with significant left ventricular dysfunction secondary to coronary artery disease, identification of the presence and extent of contractile reserve and, therefore, viable myocardium during low-dose dobutamine infusion can predict the recovery of left ventricular function after revascularization, survival rate, and future cardiac events.     

Pregnancy-induced severe left ventricular systolic dysfunction in a patient with hypertrophic cardiomyopathy

This paper reports the first case of hypertrophic cardiomyopathy (HCM) that developed postpartum congestive heart failure (CHF) and severe left ventricular (LV) systolic dysfunction. Review of the literature and clinical implications are discussed.     

Diagnosis and management of left ventricular diastolic dysfunction in the hypertensive patient

The progression of hypertensive involvement toward heart failure includes myocardial fibrosis and changes of left ventricular (LV) geometry. In the presence of these abnormalities, diastolic abnormalities occur and are defined as LV diastolic dysfunction (DD). They include alterations of both relaxation and filling, precede alterations of chamber systolic function and can induce symptoms of heart failure even when ejection fraction is normal. The prevalence of heart failure with normal ejection fraction (HFNEF) increased over time whereas the rate of death from this disorder remained unchanged. In this view, diagnosis, prognosis, and therapeutic management of DD and HFNEF in hypertensive patients is a growing public health problem. DD may be asymptomatic and identified occasionally during a Doppler-echocardiographic examination. This tool has gained, therefore, important clinical position for diagnosis of DD. Comprehensive assessment of diastolic function should be done not by a simple classification of DD progression but by estimating the degree of LV filling pressure (FP), a true determinant of symptoms and prognosis. This can be obtained by different ultrasound maneuvers/tools but the ratio between transmitral E velocity and pulsed tissue Doppler-derived early diastolic velocity (E/e' ratio) is the most feasible and accurate. The identification of left atrial enlargement may be useful in uncertain cases. The recommended management of DD in hypertensive patients should correspond to blood pressure (BP) lowering and to the attempt of reducing LV mass and normalizing LV geometry. Prospective studies with well-defined entry criteria are needed to establish whether this approach could reflect a better prognosis.     

Left ventricular apical thrombus formation in a patient with suspected tako-tsubo-like left ventricular dysfunction.

A 74-year-old woman with hypertension and bronchial asthma had chest discomfort at rest and 4 days later was admitted to her nearby hospital because of the sudden onset of right hemiparesis. The hemiparesis had almost disappeared within 24 h of onset, but because an electrocardiogram showed sinus tachycardia and diffuse symmetrical T-wave inversion, she was referred for cardiac examination. Coronary angiography did not reveal any significant coronary artery stenosis, but left ventriculography revealed severe hypokinesis of the left ventricular apical region, which contained a 4 x 4-mm solid thrombus moving freely with a wavy motion. Moreover, the activity of both protein C and protein S had decreased. The thrombus disappeared after 2 weeks of anticoagulant treatment with warfarin. Her clinical course suggested that the transient cerebral ischemic attack was caused by embolism of the left ventricular thrombus associated with 'tako-tsubo-like left ventricular dysfunction'.     

Cardiac tamponade in left ventricular dysfunction

Echocardiographic and hemodynamic data were measured in closed-chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, and 15 mm Hg) before and after production of diffuse ischemic left ventricular dysfunction. Left ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (54 +/- 3.9 mm diameter). Changes in left atrial pressure with cardiac tamponade were influenced by coexisting left ventricular dysfunction. Left atrial pressure increased with tamponade and was equal to pericardial pressure before left ventricular dysfunction was produced. However, after left ventricular dysfunction was produced, left atrial pressure was significantly higher than pericardial pressure before tamponade, but it fell toward pericardial pressure when tamponade was produced. Pulsus paradoxus (greater than 10 mm Hg) was present in all animals with cardiac tamponade before left ventricular dysfunction but in only one animal afterward. During each level of tamponade, the inspiratory fall of aortic systolic pressure was greater before than with left ventricular dysfunction. The slope of the linear regression between pericardial pressure and millimeters of mercury of inspiratory fall in aortic systolic pressure was significantly greater before than with left ventricular dysfunction (0.74 +/- 0.12 versus 0.32 +/- 0.12, p less than 0.05). Left ventricular dysfunction caused a leftward and upward shift of the pericardial pressure-volume relation. As a result, right atrial and ventricular collapse occurred with significantly smaller volumes of pericardial fluid after than before left ventricular dysfunction. We conclude that pulsus paradoxus may be absent in cardiac tamponade with coexisting left ventricular dysfunction and unequal filling pressures. Echocardiographic signs of cardiac tamponade may occur with small effusions in the presence of left ventricular dysfunction.     

Marked improvement of left ventricular function after parathyroidectomy in a hemodialysis patient with secondary hyperparathyroidism and left ventricular dysfunction.

A 52-year-old woman, a hemodialysis patient, was admitted because of exertional dyspnea. Echocardiography showed left ventricular (LV) dilatation and reduced contraction. Coronary angiography showed no fixed stenosis. She had elevated levels of parathyroid hormone (PTH) as a result of secondary hyperparathyroidism with advanced renal failure. After parathyroidectomy, marked improvement of LV function following immediate decrease of blood levels of PTH was observed. It is suggested that PTH might have a significant role in the pathogenesis of LV dysfunction and that parathyroidectomy might be effective as a therapy for heart failure in some patients with secondary hyperparathyroidism and LV dysfunction.     

Takotsubo-like transient biventricular dysfunction with pressure gradients

A 78-year-old woman was admitted to our hospital due to chest oppressive sensation. Admission electrocardiography revealed ST-segment elevation in I, II, III, aV(F) and V(2-6) leads. Left ventriculography showed apical akinesis and basal hyperkinesis with a pressure gradient of 60 mmHg between the left ventricular apex and the base. Right ventriculography also showed similar abnormal wall motion with a pressure gradient of 28 mmHg. Follow-up cardiac catheterization after 16 days showed normal wall motion with no pressure gradients. However, dobutamine stress (10 microg/kg/min) caused a pressure gradient of 60 mmHg between the left ventricular apex and the aorta.     

Hepatitis C virus infection in a patient with dermatomyositis and left ventricular dysfunction

Hepatitis C virus (HCV) infection is frequently associated with autoimmune disease. We present here a case of dermatomyositis manifested as heart failure in which HCV was detected from an endomyocardial biopsy sample. HCV infection may have contributed to the left ventricular dysfunction in this patient with dermatomyositis.     

Unrecognized left ventricular dysfunction in an apparently healthy cocaine abuse population

To determine the frequency and severity of clinically unrecognized left ventricular (LV) dysfunction related to cocaine use, 84 asymptomatic cocaine abusers underwent cardiac evaluation which included chest x-ray, electrocardiography (ECG), and radionuclide angiography after a two-week abstinence from cocaine use. LV dysfunction was discovered in 6/84 (7%). Regional wall motion abnormalities suggesting a localized myocardial abnormality were found in 2, whereas an ejection fraction less than 50% suggesting a more global process was noted in 4. An abnormal chest x-ray was found in only 1 subject and none had abnormal ECGs. In each of these cases, repeated and protracted use of cocaine was documented and the suggestion of cardiac dysfunction was supported by at least one other independent abnormal finding. In these 6 cases, the dysfunction was clinically unrecognized and unsuspected after routine evaluation. The significance of subclinical LV dysfunction in this population has not been determined and requires long-term study.     

Dual-site right ventricular and left ventricular pacing in a patient with left ventricular systolic dysfunction and atrial fibrillation using a standard CRT-D device

In patients undergoing cardiac resynchronization therapy with defibrillator (CRT-D) implantation for left ventricular systolic dysfunction (LVSD) accompanied by permanent atrial fibrillation (AF), generally, the unused atrial port is plugged at device implantation. We describe an alternative use for the atrial-port in this case report.A 43 year old gentleman with LVSD due to left ventricular non-compaction (LVNC) and AF of unknown duration underwent a CRT-D implantation after optimization of cardiac failure treatment. The atrial-port which would otherwise have been plugged was connected to a high right ventricular septal (RVS) pacing-lead and the shock-lead was positioned at the right ventricular apex (RVA). This approach permitted modified cardiac resynchronization in a high RVS to left ventricular (LV) and RVA pacing sequence using the high RVS and LV pacing combined with a shock vector including the RV apex. A standard CRT-D device with a minimum programmable A–V delay of 30 ms (technically RVS to LV delay in the ‘DDD’ pacing mode) was used. The device was programmed to a ‘DDD’ pacing mode (sequential multi-site ventricular pacing with some programmability). The mode switch operation was programmed ‘OFF’ since atrial sensing is unavailable. Device-delivered shocks did not cardiovert the patient back to sinus rhythm suggesting that the AF was permanent (no prior cardioversion attempts were made on the presumption that the chances of maintaining sinus rhythm, given the underlying cardiac condition, were low). Subsequently, the patient required radio-frequency ablation of the atrio-ventricular node for conducted AF. Symptomatic, echocardiographic and radiological improvement preceded atrio-ventricular node ablation.ConclusionAmongst AF patients with permanent AF undergoing CRT-D implantation, those patients who are likely to have the CRT-D device atrial-ports plugged could benefit from having both the options of (i) a RVA shock vector as well as (ii) a high RVS-pacing feasible, by utilizing the atrial-port of a conventional CRTD device for a RVS pacing lead, should a RVA shock-lead position be preferred. New device programming algorithms will be necessary to make patient-customized programming in this lead configuration flexible, more useful clinically and easy.