Transcatheter closure of atrial septal defect using intracardiac echocardiography: a two-center, retrospective study.

AIMS: We present the experience and long-term results of intracardiac echocardiography (ICE)-guided closure of ostium secundum atrial septal defects (ASDs) in two Italian centers and investigate its systematic applicability as the gold standard in routine clinical practice. METHODS: We retrospectively evaluated all consecutive patients who underwent an ASD percutaneous closure procedure from March 2008 to February 2020. All patients underwent a preprocedural transesophageal echocardiography (TEE) evaluation. The closures were carried out under fluoroscopic and ICE guidance. A follow-up visit was performed at 1, 3 and 12 months, followed by telephone evaluations approximately every 2 years. RESULTS: Sixty-six patients (29% male individuals), mean age 43 ±â€Š16 years, were treated. In 15 cases, the TEE defect diameter was less than 10 mm, and in 8 of these patients, the ICE intraprocedural sizing increased the maximum diameter by more than 5 mm. Sizing balloon of the defect was performed in 51 cases; 2 patients received an ASD 38 mm device. Eight patients had multiple defects; in three of these, it was necessary to apply two devices. Four patients showed nonsignificant residual shunt; no complications related to the use of ICE were observed. One patient presented the migration of the ASD device into the abdominal aorta, percutaneously retrieved with a snare. No major complications were recorded during the entire follow-up period. CONCLUSION: This study confirms that ICE monitoring during ASD percutaneous closure is well tolerated and effective; it might be achievable as a routine gold standard by operators willing to use ICE systematically in all transcatheter closure interventions of interatrial communications.

One-year results from the Assessing MICRO-vascular resistances via IMR to predict outcome in ST-elevation myocardial infarction patients with multivessel disease undergoing primary PCI (AMICRO) trial.

Background: In ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary angioplasty (PPCI) the index of microcirculatory resistance (IMR) correlates to the extent of myocardial damage and left ventricular (LV) function recovery. Data on the IMR time-course and impact on clinical outcome in STEMI patients with multi-vessel disease (MVD) are scarce. Aims: We designed a prospective, multicenter clinical trial to assess the infarct-related artery (IRA)-IMR in STEMI patients with MVD undergoing PPCI and to explore its potential in relationship with outcome and LV remodeling. Methods: The study enrolled 242 STEMI patients with MVD. Both fractional flow reserve (FFR) and IMR of the IRA were assessed after successful PPCI. Then, FFR/IMR measurements were repeated in the IRA at a staged angiography, and FFR-guided angioplasty was performed in non-IRA lesions. The primary endpoint was the composite of cardiovascular death, re-infarction, re-hospitalization for heart failure, resuscitation or appropriate ICD shock at 1-year follow-up. Results: A significant improvement of IRA-IMR values (from 47.9 to 34.2, p < 0.0001) was observed early after PPCI. Staged FFR-guided angioplasty was performed in 102 non-IRA lesions. We failed to find a correlation between IRA-IMR, clinical events and LV remodeling. Notwithstanding, in patients with anterior STEMI an inverse correlation between initial IMR values and LV function at follow-up was observed. Conclusion: After successful PPCI, a significant proportion of patients with STEMI and MVD had coronary microvascular dysfunction as assessed by IMR that recovered early after reperfusion. Higher IMR values predicted lack of improvement of LV function only in anterior STEMI. Clinical trial registration: https://clinicaltrials.gov/, identifier [NCT02325973].

Transcatheter mitral valve repair for the treatment of severe mitral regurgitation and exertional pre-syncope in a patient with non-obstructive hypertrophic cardiomyopathy: a case report.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) has a complex pathophysiology and heterogeneous phenotypic expression. In obstructive HCM with significant mitral regurgitation (MR), MitraClip device implantation reduces MR severity and symptoms. There are no data regarding MitraClip implantation in patients with non-obstructive HCM and significant MR. CASE SUMMARY: A 78-year-old woman with non-obstructive HCM and significant functional MR (3+) was admitted to our centre for dyspnoea and episodes of pre-syncope under light stress. Transthoracic and transoesophageal echocardiography showed a normal left ventricular ejection fraction and normal right heart pressures, an inverted mitral filling pattern, and a central prevalent jet (A2-P2 origin) of MR. Exercise echocardiography performed to verify exercise tolerance was interrupted at the 50-W stage due to severe hypotension and pre-syncope. After transcatheter edge-to-edge repair using the MitraClip system, the patient exhibited a reduction in MR Grade from 3+ to 1+. Follow-up up to 1-year post-procedure revealed noticeable improvements in exercise tolerance and symptoms. There were no further episodes of pre-syncope. DISCUSSION: In non-obstructive HCM, the pathophysiological role of MR in symptom generation is unknown. In this patient, we speculated that significant MR contributed to the mechanisms responsible for severe hypotension and pre-syncope during exercise. A reduction in MR after MitraClip implantation was associated with symptomatic improvements. Our findings further highlight the potential utility of the exercise stress test in therapeutic decision-making for patients with non-obstructive HCM and MR.

ECMO-Supported Ablation and Percutaneous Repair of Severe Valvulopathy: A Winning Combination in a Complex Clinical Case.

In this case report, we describe a complex case of a 67-year-old patient who was suffering from acute heart failure with electrical storm. Clinical case management was based on an integrated approach comprising two different procedures that were complementary and synergistic, and that allowed the patient to reach acute stabilization and to demonstrate mid-term clinical improvement. Complex clinical settings, such as electrical and hemodynamic instability, require complex solutions. The use of an integrated approach that allows physiopathological mechanisms to work together may be beneficial for these patients.

Spontaneous coronary artery dissection: One more extrarenal manifestation of autosomal dominant polycystic kidney disease?

Autosomal dominant polycystic kidney disease (ADPKD) may present with a variety of extrarenal manifestations. Only 1 case of spontaneous coronary artery dissection has been reported so far in ADPKD. Here we report a case of coronary artery dissection occurring in a 38-year-old woman with ADPKD and an unremarkable medical history. She was admitted to the intensive care unit with acute chest pain. Anterior myocardial infarction was diagnosed by ECG; the patient was treated with thrombolysis with tenecteplase and aspirin, heparin and carvedilol. Then she was referred to the cardiac catheterization laboratory. Coronary angiography revealed a long linear dissection in the middle left descending coronary artery (DCA) with TIMI 1 distal flow. Complete vessel recanalization was achieved by positioning 2 drug-eluting and overlapped stents in the middle DCA and a further proximal stent due to residual proximal dissection, resulting in a TIMI 3 distal flow. There were no procedural complications, and the patient was discharged on day 8. In conclusion, spontaneous coronary artery dissection is a rare cause of myocardial ischemia and infarction. Myocardial infarction in patients without any risk factors for coronary atherosclerosis or in young patients should prompt a diligent search for a possible spontaneous coronary artery dissection. It is suggested that ADPKD may be a predisposing factor for spontaneous coronary artery dissection.

Optical coherence tomography imaging in complicated acute myocardial infarction treated with primary angioplasty and AngioJet.

We describe the case of a 47-year-old man presenting with inferior acute myocardial infarction complicated by complete atrioventricular block and cardiogenic shock, who underwent primary angioplasty and rheolytic thrombectomy with AngioJet and subsequent evaluation by optical coherence tomography. Optical coherence tomography is a rather novel technique in the management of coronary disease, and as far as we know, this is the first report about optical coherence tomography imaging after AngioJet thrombectomy. Moreover, we provide a brief discussion on advantages and disadvantages of this imaging modality on the basis of current practice.

Alpha- and beta-adrenergic receptor polymorphisms in hypertensive and normotensive offspring.

BACKGROUND: The offspring of hypertensive families are characterized by higher arterial blood pressure values and a depressed autonomic control of heart rate. The present study aimed to verify whether these differences are associated with a different genotype distribution of functionally relevant polymorphisms of the alpha- and beta-adrenergic receptor (AR) genes. METHODS: We selected 109 age- and sex-matched young normotensive subjects with (FH+, n = 56) and without (FH-, n = 53) a family history of hypertension who underwent evaluation of arterial pressure; 24-h electrocardiogram monitoring to assess time-domain parameters of autonomic heart rate control [i.e. mean RR interval (NN), SD of RR intervals (SDNN) and mean square root of the differences of consecutive RR intervals (rMSSD)]; spectral baroreflex sensitivity measurement; and echo-Doppler to assess diastolic function and left ventricular mass. They were also characterized for the following polymorphisms by means of polymerase chain reaction-restriction fragment polymorphism analysis: Arg492Cys in the alpha1a-AR; Del301-303 in the alpha2b-AR; Ser49Gly and Arg389Gly in the beta1-AR; and the 5' leader cistron Arg19Cys, Arg16Gly and Gln27Glu in the beta2-AR. RESULTS: FH+ individuals showed a higher systolic pressure, a lower SDNN and a greater isovolumic relaxation time compared to normotensive offspring. No differences were found between the two groups when genotype distribution of the studied polymorphisms was considered. Subjects carrying alpha1a-AR Cys492 allelic variant showed lower values of NN, SDNN and rMSSD, independent of age, gender and body mass index. CONCLUSIONS: The functionally relevant polymorphisms of alpha2b-, beta1- and beta2-AR genes are not associated with a family history of essential hypertension. The Arg492Cys polymorphism of the alpha1a-AR gene, although not associated with a family history of hypertension, was strongly related to autonomic control of heart rate.

Allelic variants of natriuretic peptide receptor genes are associated with family history of hypertension and cardiovascular phenotype.

OBJECTIVE: Abnormalities in the natriuretic peptide system could play a key role in the genesis of hypertension. We evaluated the associations between a family history of hypertension, cardiovascular phenotype and allelic variants of Npr1 and Npr3, two candidate genes that codify for natriuretic peptide receptors. METHODS: We genotyped 45 young normotensive subjects (19 males, 26.8 +/- 3.7 years) with accurately assessed family history of hypertension (FH+) and 52 (26 males, 26.1 +/- 3.1 years) without (FH-) for the known variants of Npr1 and Npr3 genes, and for a novel length difference (3C/4C) polymorphism at position 15129 in the 3'-untranslated region of the Npr1 gene. Blood pressure, echocardiography and plasma brain natriuretic peptide were assessed. RESULTS: Both the novel Npr1 3C allele (59 versus 33%, P < 0.001) and the 3C/3C genotype (31 versus 8%; P < 0.001) were significantly more frequent in FH+ than in FH-. The inverse distribution of the 4C/4C genotype suggested that a casual association was very unlikely. Moreover, the 3C/3C homozygous had significantly higher systolic blood pressure (121.1 +/- 6.3 versus 115.6 +/- 7.8 mmHg in 4C/4C; P < 0.05) and a longer left ventricular isovolumic relaxation time (67 +/- 10 versus 61 +/- 9 ms; P < 0.05). The Npr3 C(-55) allele variant was also more frequent in FH+ (88 versus 76%, P < 0.05), but was not associated with the cardiovascular phenotype. CONCLUSIONS: The novel Npr1 gene 3C variant and the Npr3 gene C(-55) allele are associated with hypertensive family history. Moreover, the functional Npr1 3C variant, when homozygous, is also associated with higher systolic blood pressure and prolonged ventricular relaxation.

[Natriuretic peptides and essential arterial hypertension]. / Peptidi natriuretici e ipertensione arteriosa essenziale.

Natriuretic peptide system plays a well-defined role in the regulation of blood pressure and fluid volume. Although the effects of natriuretic peptides (atrial natriuretic peptide, brain natriuretic peptide and C-type natriuretic peptide) are mediated by specific biologic receptors, their plasma level is influenced by clearance receptors. It has been demonstrated that in hypertensive subjects plasma levels of natriuretic peptides are impaired; furthermore peptide receptor polymorphisms have been shown to be significantly associated with hypertension and cardiac hypertrophy. Studying normotensive subjects at high genetic risk of developing hypertension on the basis of family history makes it possible to investigate the role of natriuretic peptide system in the genesis of hypertension. It has been shown that plasma atrial and ventricular natriuretic peptide levels are significantly reduced in normotensive subjects with a family history of hypertension. Our study is the first one showing association among positive family history of essential hypertension and natriuretic peptide receptor polymorphisms. We identified a novel insertion/deletion polymorphism at position 15,129 in the 3'-untranslated region (3'-UTR) of NPRA receptor mRNA. The NPRA gene deletion variant is associated with hypertensive family history and higher systolic blood pressure. The "deletion 15129" variant might participate in the functional impairment of natriuretic peptide system defining an increased genetic susceptibility to hypertension.