Structural Heart Disease Emergencies

2020 ◽  
pp. 088506662091877
Author(s):  
Jacob C. Jentzer ◽  
Bradley Ternus ◽  
Mackram Eleid ◽  
Charanjit Rihal

Structural heart disease (SHD) emergencies include acute deterioration of a stable lesion or development of a new critical lesion. Structural heart disease emergencies can produce heart failure and cardiogenic shock despite preserved systolic function that may not respond to standard medical therapy and typically necessitate surgical or percutaneous intervention. Comprehensive Doppler echocardiography is the initial diagnostic modality of choice to determine the cause and severity of the underlying SHD lesion. Patients with chronic SHD lesions which deteriorate due to intercurrent illness (eg, infection or arrhythmia) may not require urgent intervention, whereas patients with an acute SHD lesion often require definitive therapy. Medical stabilization prior to definitive intervention differs substantially between stenotic lesions (aortic stenosis, mitral stenosis, left ventricular outflow tract obstruction) and regurgitant lesions (aortic regurgitation, mitral regurgitation, ventricular septal defect). Patients with regurgitant lesions typically require aggressive afterload reduction and inotropic support, whereas patients with stenotic lesions may paradoxically require β-blockade and vasoconstrictors. Emergent cardiac surgery for patients with decompensated heart failure or cardiogenic shock carries a substantial mortality risk but may be necessary for patients who are not eligible for catheter-based percutaneous SHD intervention. This review explores initial medical stabilization and subsequent definitive therapy for patients with SHD emergencies.

2013 ◽  
Vol 304 (12) ◽  
pp. H1644-H1650 ◽  
Author(s):  
Lori A. Walker ◽  
David A. Fullerton ◽  
Peter M. Buttrick

Human heart failure has been associated with a low level of thin-filament protein phosphorylation and an increase in calcium sensitivity of contraction relative to both “control” human heart tissue and tissue from small animal models. However, diverse strategies of human tissue procurement and the reliance on tissue obtained from subjects with end-stage heart failure suggest this may be an incomplete characterization. Therefore, we evaluated cardiac left ventricular (LV) biopsy samples from patients with aortic stenosis undergoing valve replacement who presented either with LV hypertrophy and preserved systolic function (Hyp) or with LV dilation and reduced ejection fraction (Dil). In Hyp, total troponin I (TnI) phosphorylation was markedly increased and myosin light chain 2 (MLC2) phosphorylation was unchanged relative to a control group of patients with normal LV function. Conversely, in Dil, total TnI phosphorylation was significantly reduced compared with control subjects and MLC2 phosphorylation was increased. Site-specific analysis of TnI phosphorylation revealed phenotype-specific differences such that Hyp samples demonstrated significant increases in phosphorylation at serine 22/23 and Dil samples had significant decreases at serine 43. The ratio of phosphorylation at the two sites was biased toward serine 22/23 in Hyp and toward serine 43/45 in Dil. Western blot analysis showed that protein phosphatase-1 was reduced in Hyp and protein phosphatase-2 was reduced in Dil. These data suggest that posttranslational modifications of sarcomeric proteins, both singly and in combination, are stage specific. Defining these changes in progressive heart disease may provide important diagnostic and treatment information.


2010 ◽  
pp. 2728-2728
Author(s):  
Andrew L Clark ◽  
John G. F Cleland

Presentations of acute heart failure fall into three overlapping categories: (1) acute breathlessness and pulmonary oedema, (2) chronic fluid retention and peripheral oedema (anasarca), and (3) cardiogenic shock. Examination features include tachycardia, hypotension, a raised venous pressure, basal crackles, and peripheral oedema. Auscultation may reveal a third heart sound or features of precipitating valvular heart disease. Initial management focuses on confirming the diagnosis and identification of the immediate precipitant (e.g. arrhythmias, myocardial infarction, decompensating valvular heart disease). Initial investigations include a 12-lead electrocardiogram (ECG), chest radiograph, full blood count, biochemical screen, troponin and thyroid function. Brain natriuretic peptide (BNP) is useful in confirming the diagnosis where clinical features are present and a normal BNP is helpful in excluding the diagnosis. All patients should undergo echocardiographic assessment early in the course of a hospital admission to assess left ventricular function and to look for underlying valvular heart disease. In patients with acute pulmonary oedema investigation and management should proceed simultaneously. Intravenous loop diuretics and nitrates are commonly used therapies and may be combined with ventilatory support with oxygen and continuous positive airways ventilation. Mechanical support may be appropriate as a bridge to definitive therapy in potentially reversible causes. Inotropes are often used but without convincing evidence that they improve outcome. In patients with features are of peripheral oedema and low cardiac output, fluid retention (usually >5 litres) is the predominant feature. Management is principally with bed rest, loop diuretics (usually by intravenous infusion), and, where appropriate, aldosterone antagonists. Thiazide diuretics can be added in resistant cases. Prophylactic low molecular weight heparin should be prescribed. Careful monitoring of fluid balance with daily weights and daily electrolytes is essential. Angiotensin converting enzyme (ACE) inhibitors and subsequently β‎-blockade can be introduced once a satisfactory diuresis has been achieved. Management of cardiogenic shock is usually determined by the cause. Fluid status should be assessed and an adequate left ventricular filling pressure ensured by the administration of intravenous fluids where required (particularly in the case of right ventricular infarction). Revascularization is the mainstay of therapy in acute myocardial infarction. Circulatory support with intra-aortic balloon counter-pulsation (IABP), inotropic agents, ventricular assist devices (VADs), and extracorporeal membrane oxygenation should be considered for reversible causes (e.g. ventricular septal rupture, papillary muscle rupture, acute myocarditis and postpartum cardiomyopathy). Hospital admission with acute heart failure caries a poor prognosis with an average in-hospital mortality of 10–15% rising to up to 60% at 30 days in cases of cardiogenic shock.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
M Lembo ◽  
V Fazio ◽  
V Capone ◽  
L Esposito ◽  
R Sorrentino ◽  
...  

Abstract Background Hyperuricemia has been reported to accelerate the occurrence and worsening of cardiovascular disease, being a risk factor for coronary heart disease and cardiac mortality. Elevated uric acid (UA) is also associated with left ventricular (LV) hypertrophy and with LV diastolic dysfunction. The effect of hyperuricemia (HU) on LV systolic function is still unclear. Purpose Aim of our study was to evaluate the impact of elevated UA serum levels on LV systolic function, also evaluating longitudinal deformation, in a population of hypertensive patients. Methods We enrolled 160 treated hypertensive patients (M/F = 104/56, age 58.2 ± 13.3 years, blood pressure = 136.7 ± 16.8/81.3 ± 10.9 mmHg), who underwent standard echo-Doppler exam, including speckle tracking quantification of global longitudinal strain (GLS, considered in absolute value). HU was defined as UA≥7 mg/dL and the study population was divided in two groups: patients with (n = 63) and without (n = 97) HU. Exclusion criteria were coronary artery disease, overt heart failure, hemodynamically significant valve heart disease, primary cardiomyopathies, permanent atrial fibrillation and inadequate echo imaging. Results The two groups were comparable for sex prevalence, blood pressure and heart rate. Patients with HU were older and had higher body mass index (BMI) (both p < 0.0001). Prevalence of diabetes mellitus was higher in the group of patients with HU than in patients with normal UA (69% vs. 12% p < 0.0001). Fasting glycaemia was higher (p < 0.0001) and glomerular filtration rate (GFR) lower in HU hypertensives (both p < 0.0001). LV mass index (LVMi) was higher in patients with HU (p < 0.0001). Among diastolic parameters, transmitral E/A ratio (p < 0.0001) was lower, whereas E/e’ ratio (p < 0.0001), E velocity deceleration time and left atrial volume index (both p < 0.001) were higher in HU hypertensives. GLS resulted to be lower in patients with HU (20.8 ± 1.5 vs. 22.3 ± 2.2%, p < 0.0001). LV ejection fraction, despite still in normal range values, was also slightly lower in comparison with controls (60.6 ± 4.0 vs. 62.2 ± 3.9%, p < 0.01). Serum UA levels resulted to be negatively correlated with GLS (r=-0.28, p < 0.0001) (Figure), but not with ejection fraction. By a multiple linear regression analysis performed in the pooled hypertensive population, after adjusting for age, BMI, GFR, fasting glycaemia and LVMi, the association between UA levels and GLS remained significant (standardized beta coefficient =-0.25, p < 0.01), besides the significant impact of age (beta=-0.19 , p < 0.05). Conclusions In hypertensive patients with multiple cardiovascular risk factors, the presence of HU is associated with LV diastolic and systolic dysfunction. Serum UA levels and GLS resulted independently associated even after adjusting for several clinical and echo confounders. Acid uric might be considered as an independent marker of early LV dysfunction, able to identify hypertensive patients at increased risk for heart failure. Abstract P658 Figure. Relation between uric acid and GLS


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hideki Okui ◽  
Shuichi Hamasaki ◽  
Sanemasa Ishida ◽  
Masakazu Ogawa ◽  
Keishi Saihara ◽  
...  

Background: The coronary microvascular vasodilating function is an important determinant of patient outcomes in a number of clinical settings, including coronary artery disease, hypertensive heart disease, or cardiomyopathy. However, the characteristics or the implication of coronary microcirculation in valvular heart disease has not been fully elucidated. The present study was designed to assess coronary vasodilating function and its effects on systolic function in patients with aortic regurgitation (AR) and mitral regurgitation (MR). Methods: Forty-four consecutive patients (66 yrs) with moderate to severe AR and 45 consecutive patients with moderate to severe MR (64 yrs) were enrolled for this study. All patients were free of coronary artery stenosis. Fifty-one age-matched patients without underlying cardiovascular disease served as controls. Endothelium-dependent and endothelium-independent vasodilating function of resistance coronary artery were assessed by coronary blood flow (CBF) response to acetylcholine and papaverine, respectively. Left ventricular ejection fraction (LVEF) was determined by echocardiography as an indicator of systolic function. Results: In patients with AR, both %change in CBF response to acetylcholine and papaverine were significantly lower than controls (32 ± 61 vs 64 ± 84, 172 ± 87 vs 268 ± 105, p < 0.05, p < 0.01, respectively). Further, %change in CBF response to acetylcholine positively correlated with LVEF (r = 0.45, p < 0.01). In patients with MR, %change in CBF response to papaverine was significantly lower than controls (221 ± 123 vs 268 ± 105, p < 0.05), but %change in CBF response to acetylcholine was comparable with controls. Moreover, neither %change in CBF response to acetylcholine nor CBF response to papaverine had significant correlation with LVEF. Conclusion: In patients with AR, both endothelium-dependent and endothelium-independent vasodilating function of resistance coronary artery were deteriorated. Further, endothelium-dependent vasodilating function may be associated with left ventricular systolic function. Our findings indicate coronary microvascular endothelial dysfunction as a potential target for prevention of systolic heart failure in patients with AR.


2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Giulia Stronati ◽  
Alessia Urbinati ◽  
Giuseppe Ciliberti ◽  
Alessandro Barbarossa ◽  
Umberto Falanga ◽  
...  

Abstract Aims Tachycardiomyopathy (TCM) is a reversible cause of left ventricular dysfunction, secondary to rapid and/or asynchronous, irregular myocardial contraction. The disease can be divided in two main subgroups: arrhythmia-induced TCM also known as pure TCM, where the arrhythmia is the sole reason for the dysfunction, and impure TCM also known as arrhythmia mediated TCM, where the arrhythmia can exacerbate or worsen heart failure (HF) or an underlying heart disease. Pure TCM has already been described as affecting almost 1 out of 10 patients admitted for de novo acute HF. The aim of our study was to compare pure TCM and de novo acute HF and structural heart disease patients in terms of mortality and cardiovascular (CV)-related hospitalizations. Methods and results Prospective, observational study enrolling all consecutive patients with a confirmed diagnosis of TCM and all patients admitted for de novo acute HF. The TCM diagnosis was suspected in all patients admitted for HF-related symptoms, an ejection fraction &lt;50% with concomitant persistent atrial or ventricular arrhythmia, and confirmed after clinical and echocardiographic recovery. Acute HF diagnosis was made in all patients with an ejection fraction &lt;50%, new HF-like symptoms, diagnosis of structural heart disease and no evidence of clinical or echocardiographic recovery. For each patient, all-cause death and CV-related hospitalizations were recorded. One-hundred-and-ten patients with TCM (61.8% males, 68 ± 13 years old) were propensity matched with a control population of patients with HF and structural heart disease (76.6% males, 71 ± 15 years old, 75% ischaemic heart disease). After a median follow-up of 5.1 years (1st–3rd quartile 2.6–7.0 years) TCM patients showed an overall higher estimate of survival when compared to HF patients (78% vs. 58%; P = 0.031; Figure 1A) but a lower estimate of time free from CV-related hospitalization (31% vs. 57%, P = 0.014; Figure 1B). TCM patients got most often readmitted for AF-related elective procedures (60.8% of all hospitalizations) such ablation procedures or elective cardioversion, TCM recurrence (13.7%), and elective coronary angiography (5.9%). On the other hand, HF patients got readmitted for HF worsening (40.9%), cardiac or vascular surgery (22.7%), and elective coronary angiography (9.1%). Propensity-score matched analysis confirmed the results for all-cause death (81% vs. 49%; P = 0.006) and CV-related hospitalizations (29% vs. 54%; P = 0.007). Conclusions TCM is associated with higher rate of survival when compared to de novo acute HF, even after propensity score adjustment. On the other hand, patients with TCM got readmitted more frequently, requiring more often elective procedures in order to control the triggering arrhythmia.


2018 ◽  
Vol 4 (2) ◽  
pp. 78 ◽  
Author(s):  
Tomaz Podlesnikar ◽  
Victoria Delgado ◽  
Jeroen J Bax ◽  
◽  
◽  
...  

Valvular heart disease (VHD) and heart failure (HF) are major health issues that are steadily increasing in prevalence in Western populations. VHD and HF frequently co-exist, which can complicate the accurate diagnosis of the severity of valve stenosis or regurgitation and affect decisions about therapeutic options. Transthoracic echocardiography is the first-line imaging modality to determine left ventricular (LV) systolic function, to grade valvular stenosis or regurgitation and to characterise the mechanism underlying valvular dysfunction. 3D transoesophageal echocardiography, cardiovascular magnetic resonance and cardiac CT are alternative imaging modalities that help in the diagnosis of patients with HF and VHD. The integration of multimodality cardiovascular imaging is important when deciding whether the patient should receive transcatheter aortic valve repair and replacement therapies. In this article, the use of multimodality imaging to diagnose and treat patients with VHD and HF is reviewed.


Author(s):  
Siddiq Ibrahim Khalil ◽  
Suha Khalil ◽  
Hajir Khalid Albadri ◽  
Mohamed Khalid Ali ◽  
Hiba Abdalla Albashir ◽  
...  

<p><strong> </strong></p><p>Heart failure is a rapidly growing cardiovascular (CV) problem in Sudan due to affluence and lifestyle changes producing high rates of CV risk factors and consequent coronary heart disease in addition to the historical causes of hypertension and rheumatic heart disease.</p><p>This study is intended to measure the prevalence of heart failure (HF) among hospital admissions and study the recent trends in etiology, clinical features and methods of treatment.</p><p>Methods: All admissions at Sudan Heart Institute between January 2000 and June 2011 were studied. Patients went through detailed history taking and physical examination. Investigations included 12 lead ECG and chest X-ray, echocardiography and cardiac catheterization was also carried out where indicated.</p><p>Results: A total of 12453 cases were collected and 1073 were verified by the authors and an independent cardiologist, constituting 8.6% of CV disease admissions. Female to male ratio was 1:1.6 and age 15 to 96 years (median 58 years). 74.6 % of all patients were urban dwellers. Left ventricular (LV) systolic dysfunction accounted for 71.6% and preserved systolic function 28.4%.  Ischemic aetiology accounted for 44.6% of cases, hypertension 24.8 %, RHD 14.4% and idiopathic 12.4%. </p><p>Conclusion: Ischemic cardiomyopathy emerged as the main cause of HF among urban population probably due to changes in lifestyle. Treatment and prevention of these risk may reduce the prevalence of heart failure. </p>


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