Severe Impairment Of Left Ventricular Function Research Articles

A VENTRICULAR TACHYCARDIA CASE NOT TREATABLE WITH TRANSCATHETER ABLATION DUE TO APICAL THROMBOSIS OF THE LEFT VENTRICLE RESOLVED WITH RADIOTHERAPY BASED ON THE NON–INVASIVE MAPPING SYSTE

Abstract The clinical case focuses on a 52–year–old man smoker, heavy alcohol consumer. In 2017 he began with sustained ventricular tachycardia (VT) effectively treated with DC–shock. The following ECG showed signs of anterior necrosis. Severe left ventricular (LV) dilatation, apical thrombosis and severe impairment of LV function were found on echocardiogram. Angiography was performed and LAD occlusion was found. Since of 68% necrosis of the LV at myocardial scintigraphy, no revascularization was performed. He underwent to a dual chamber ICD implantation and started oral anticoagulation therapy. In the following years recurrence of arrhythmic episodes, despite the optimization of antiarrhythmic therapy, led the patient to numerous hospitalizations. Unfortunately the persistence of the apical thrombosis, made transcatheter ablation NOT possible. The only chance for the patient remained stereotactic arrhythmia radioablation. But which area of the LV to highlight as responsible for the arrhythmia and how to program the radiotherapy treatment plan was a challenging problem. We proposed in March 2023 non–invasive mapping of arrhythmia using Cardioinsight. The patient performed heart high–resolution computed tomography (CT) for the anatomical reconstruction with precise spatial resolution of all LV aereas and surrounding structures. A 252–electrode vest is applied to the patient’s torso and connected to the system Cardioinsight. A programmed ventricular stimulation was performed using ICD inducing two VT morphologies. Through electroanatomical mapping we identified the mid LV antero–septal and infero–septal sites as target areas. Thanks to multidisciplinary team a personalized treatment plan was created to deliver an effective lesion in the target area and minimize exposure to nearby organs at risk. The treatment was generated, optimized and delivered by TrueBeam, lasted 3 minutes and no complications arose. The patient was quickly discharged in good clinical condition. After 3 months of clinical well–being he was hospitalized for a single episode of VT. Up to now no hospitalizations occurred. This treatment may represent a "bail–out" choice in patients with advanced heart failure with arrhythmic storm who have exhausted all other therapeutic options.

Clinical characteristics and long-term outcomes in patients with peripartum cardiomyopathy (PPCM) receiving left ventricular assist devices (LVAD).

Peripartum cardiomyopathy (PPCM) is a rare cause of heart failure (HF), presenting with left ventricular (LV) systolic dysfunction either at the end of pregnancy or in the months following delivery. In rare cases, PPCM leads to severe impairment of LV function, refractory cardiogenic shock or advanced HF. LV assist devices (LVAD) have been shown to be a feasible treatment option in advanced HF. However, little is known about long-term outcomes and prognosis of PPCM patients undergoing LVAD implantation. A retrospective analysis of data from PPCM patients undergoing LVAD implantation in two tertiary centers with respect to long-term outcomes was performed. Twelve patients of median age 30 (18-39) years were included. Eight patients were experiencing cardiogenic shock (INTERMACS 1) at implantation. Seven patients were implanted within 1 month of their PPCM diagnosis. Median duration of LVAD support was 19 (2-92) months with median follow up of 67 (18-136) months (100% complete). In-hospital and 1-year mortality were 0% and 8.3%, respectively. Two patients died on LVAD support, four patients were successfully bridged to transplantation, two patients are still on LVAD, and four were successfully weaned due to sufficient LV recovery (one died after LV function deteriorated again). LVAD treatment of decompensated end-stage PPCM is feasible. Early LVAD provision led to hemodynamic stabilization in our cohort and facilitated safe LV recovery in one third of these young female patients.

Prophylactic Epicardial Left Ventricular Lead Implantation for Biventricular Pacing During Operations

Surgical epicardial left ventricular (LV) lead implantation for biventricular pacing has advantages over the transvenous approach in cardiac surgical patients. We investigated the benefit of concomitant prophylactic LV lead implantation during open heart operations and subsequent lead performance after patients with impaired LV function receive a biventricular device. Retrospective data of 4,844 patients undergoing cardiac operations through a sternotomy between January 2001 and December 2011 were analyzed. Of these, 380 patients (7.8%) had severe impairment of LV function (contrast left ventriculogram showing grade 4 estimated ejection fraction or echocardiogram showing LV ejection fraction<0.30). LV lead implantation was performed in patients in whom recovery of LV function was unlikely. Lead performance data were collected at follow-up. LV lead implantation occurred in 95 patients (25%), and 29 (30.5%) subsequently received a biventricular device. Of patients with impaired LV function, more patients with prophylactic LV leads underwent biventricular implant than those without LV leads (30.5% vs 1.1%, p<0.0001). The median interval from LV lead implantation to connection to a biventricular device was 30 days (interquartile range, 5.5 to 145 days). At a median follow-up of 437.5 days (interquartile range, 13.8 to 1198 days), the mean pacing threshold (1.25±0.46 vs 1.58±0.66 volts, p=0.069) and impedance (383.81±70.33 vs 448.6±200.1 Ohms, p=0.168) remained stable compared with time of biventricular device connection. A significant proportion of patients with poor LV function undergoing cardiac operations may benefit from concomitant LV lead implantation. Subsequent lead performance appears satisfactory. Epicardial LV lead placement is easily accomplished during open heart operations and should be considered before the operation.

Identification of a missense mutation in the melusin-encoding ITGB1BP2 gene in a patient with dilated cardiomyopathy

In a heterogeneous cohort of patients (n=255) with sporadic and familial dilated cardiomyopathy (DCM), we searched for novel disease-associated mutations in the human melusin-encoding ITGB1BP2 gene and found only one missense mutation, which was a substitution of alanine for glycine at position 313 located in the carboxy-terminal spacer region of the molecule. This point mutation (c.938C>G) was identified in a 45-year-old male with familial DCM and severe impairment of left-ventricular function, but was absent in 300 healthy control subjects. However, its functional significance in the context of heart failure is unclear, as this amino acid substitution was predicted to be without disease-causing effects. In this report, we confirm the low prevalence of mutations and single nucleotide polymorphisms in the coding sequence of the human melusin gene in patients with DCM, ruling out the possibility that genetic variations in this myocardially transcribed gene may have a significant impact on the epidemiology of DCM-induced heart failure.

The Reliability of Echocardiographic Left Ventricular Wall Motion Index to Identify High‐Risk Patients for Multicenter Studies

To study whether the use of echocardiographic left ventricular (LV) wall motion index (WMI) is a dependable parameter for identifying patients with LV dysfunction to be enrolled in multicenter trials. Videotaped echocardiographic examinations from 200 randomly selected patients that were screened for inclusion into the DIAMOND-CHF and DIAMOND-MI trials were reevaluated by an external expert echocardiographer. WMI was calculated using the 16-segment LV model. The external echocardiographer systematically found lower values of WMI than the core laboratory. The average difference in WMI was 0.18 (SD: 0.33) in the DIAMOND-CHF trial and 0.09 (SD: 0.33) in the DIAMOND-MI trial. The difference in WMI exceeded 0.33 in 34% of the patients in both trials. The cutoff value for inclusion into the DIAMOND trials was WMI < or = 1.2. There was an agreement on WMI dichotomized to below or above 1.2 in 82% of the patients in both trials (kappa coefficient 0.66 for the DIAMOND-CHF and 0.55 for the DIAMOND-MI). Despite substantial interlaboratory variation in WMI in individual patients and a systematic lower WMI score by the external echocardiographer there was an acceptable overall agreement for identifying patients with severe impairment of LV function. This not only underscores the value of LV-WMI as a useful tool for selecting high-risk patients to be included in multicenter studies but also serves to warn against the use of rigid cutoff values for WMI in the treatment of individual patients.

Heart failure

Heart failure

Hemodynamic effects of nifedipine given alone and in combination with atenolol in patients with impaired left ventricular function

The acute intravenous (IV) (0.1, 0.2 and 0.4 μg/kg/min over 10 minutes each) and chronic oral (60 mg/day) administration of nifedipine was examined in 9 patients with significantly impaired left ventricular (LV) function (ejection fraction [EF] on radionuclide scannin was 0.20 to 0.40) who were already receiving β-blocker therapy (>25% reduction in peak exercise heart rate) with atenolol, 100 to 200 mg/day. The mean control LV end-diastolic pressure (EDP) at cardiac catheterization and EF for the group as a whole were 30 ± 3 mm Hg (range 20 to 42) (mean ± standard error of the mean) and 28.5 ± 2.4%, respectively. Three of the 9 patients had hemodynamic deterioration and LV failure at some. stage during the study, and their mean LVEDP and EF were 38 ± 3 mm Hg (range 33 to 42) and 22.6 ± 2.7%, respectively. In the 6 patients who tolerated the full treatment protocol, the mean LVEDP and EF were 26.5 ± 2.0 mm Hg (range 20 to 35) and 31.5 ± 2.8%, respectively. Seven patients received IV nifedipine, which had a negative inotropic action but did not precipitate cardiac decompensation. Chronic oral administration of nifedipine in combination with atenolol precipitated LV failure only in those with the lowest EF and highest LVEDP; usually LV failure was present with atenolol alone. Extensive infarction, frequently complicated by LV failure at the time, LVEDP >32 mm Hg and control resting EF <30 % were associated with LV failure. Removal of sympathetic nervous system support for the impaired ventricle by β blockade may be the decisive factor in precipitating hemodynamic deterioration in patients with severe impairment of LV function.

Hemodynamic effects of nifedipine during upright exercise in stable angina pectoris and either normal or severely impaired left ventricular function

The immediate effects of sublingual nifedipine (20 mg) were evaluated in 18 men with stable, exercise-related angina pectoris and angiographically confirmed coronary artery obstructions, stratified at the time of left ventricular (LV) angiography according to the degree of LV dysfunction supine at rest (Group 1: n = 9, left ventricular end-diastolic pressure [LVEDP] < 20 mm Hg; Group 2: n = 9, LVEDP > 20 mm Hg). At rest, in the upright posture in both groups, nifedipine reduced the systemic vascular resistance (p < 0.01). The systemic arterial mean (p < 0.05) and diastolic (p < 0.01) pressures were reduced despite an increase in the cardiac output (p < 0.05). Heart rate was increased only in Group 1 (p < 0.05). Pulmonary artery occluded pressure was unchanged in both groups. During upright bicycle exercise in all patients, compared to control measurements, systemic arterial pressure (p < 0.01) and vascular resistance (p < 0.05) were similarly reduced, while exercise cardiac output response and LV filling pressure did not change after nifedipine. Heart rate was increased in Group 1 (p < 0.05) and decreased in Group 2 (p < 0.05). Stroke volume during exercise after nifedipine decreased 1 ml/m 2 in Group 1 ( p > 0.05) and increased 2 ml/m 2 in Group 2 (p > 0.05) compared to control measurements; the between-group difference in the exercise heart rate and stroke volume responses after nifedipine were significant at the 5% level. These results indicate that in our patients with coronary heart disease, the major hemodynamic effect of nifedipine was systemic arteriolar dilatation. In Group 1, failure of the reduction in LV pressure work to improve cardiac output and stroke volume during exercise may reflect some degree of negative inotropic activity of the drug, particularly in view of the evidence of reflex sympathetic stimulation of the heart (tachycardia). However, patients in Group 2, with more severe impairment of LV function, showed no hemodynamic evidence of further cardiac depression following nifedipine. These results indicate that nifedipine did not further impair cardiac pumping activity even in patients with severe LV dysfunction.