Angel López-Candales

Role of Baseline Echocardiography in the Preoperative Management of Liver Transplant Candidates

Liver transplantation (LT) has not traditionally been offered to patients with intracardiac shunts (ICSs) or pulmonary hypertension (PH). There is a paucity of data regarding cardiac structural characteristics in LT candidates. We examined echocardiographic characteristics and their role in managing LT candidates diagnosed with ICS and PH. We identified 502 consecutive patients (318 men, mean age 55 ± 11 years) who underwent LT and had preoperative echocardiogram. Demographics, cardiovascular risk factors, and echocardiographic variables were recorded and data were analyzed for end-stage liver disease diagnosis. ICSs were diagnosed with contrast echocardiography and PH was defined as estimated pulmonary artery systolic pressure >40 mm Hg. Primary end points included short-term (30-day) and long-term (mean 41-month) mortalities and the correlation between pre- and perioperative stroke. In our studied population >50% had >2 cardiovascular risk factors and with increasing frequency ICSs were diagnosed in 16%, PH in 25%, and intrapulmonary shunts in 41% of LT candidates. There was no correlation between short- and long-term mortality and ICS (p = 0.71 and 0.76, respectively) or PH (p = 0.79 and 0.71). Importantly, in those with ICS, no strokes occurred. In conclusion, structural differences exist between various end-stage liver disease diagnoses. ICSs diagnosed by echocardiography are not associated with an increased risk of perioperative stroke or increased mortality. A diagnosis of mild or moderate PH on baseline echocardiogram is not associated with worse outcomes and requires further assessment. Based on these findings, patients should not be excluded from consideration for LT based solely on the presence of an ICS or PH.

Essential echocardiographic evaluation in patients with suspected pulmonary hypertension: an overview for the practicing physician

ABSTRACT Prompt and accurate diagnosis of patients presenting with symptoms suggestive of pulmonary arterial hypertension (PAH) is of outmost importance as delays in identifying this clinical entity have detrimental effects on both morbidity and mortality. Initial noninvasive assessment of these patients has traditionally included a number of routine tests of which transthoracic echocardiography (TTE) has been shown to either confirm the presence of structural anomalies of the right ventricle (RV) indicative of PAH or exclude other potential causes of pulmonary hypertension (PH). Consequently, TTE has become a well-validated and readily available imaging tool not only used for this initial screening but also for routine follow-up of PH patients. Since chronic PH is known to unbalance the normal hemodynamic and mechanical homeostatic interaction between the RV and pulmonary circulation; the resulting response is that of an abnormal RV remodeling, clinically translated into progressive RV hypertrophy and dilatation. An enlarged and hypertrophied RV not only would eventually lose effective contractility but also this gradual decline in RV systolic function is the main abnormality in determining adverse clinical outcomes. Therefore, it is of outmost importance that TTE examination be comprehensive but most importantly accurate and reproducible. This review aims to highlight the most important objective measures that can be routinely employed, without added complexity, that will certainly enhance the interpretation and advance our understanding of the hemodynamic and mechanical abnormalities that PH exerts on the RV.

The clinical dilemma of heart failure with preserved ejection fraction: an update on pathophysiology and management for physicians

The prevalence of heart failure with preserved ejection fraction (HFpEF) continues to grow at alarming rates and is predicted to become the most prevalent phenotype of heart failure over the next decade. Recent data show a higher non-cardiac comorbidity burden associated with HFpEF, and similar overall hospitalisation rates when compared with patients with heart failure with reduced ejection fraction (HFrEF). Unfortunately, clinicians mainly focus their efforts in diagnosis of HFrEF despite HFpEF accounting for 50% of the cases of heart failure. Therefore, this review is intended to create awareness on the pathophysiology, risk factors, diagnosis and management of patients with HFpEF and its core mechanical abnormality left ventricular diastolic dysfunction. Clinical distinction between HFpEF and HFrEF should be of particular interest to internal medicine physicians and general practitioners as this distinction is seldom made and early diagnosis can lag if appropriate risk factors are not promptly recognised.

Importance of the Hispanic heritage regarding diagnosis and management of hypertension

Abstract Hypertension (HTN) is a very prevalent and growing clinical problem that is not always promptly diagnosed and ∼6% of US adults remain undiagnosed. Though numerous risk factors have been linked to the development of HTN, ethnicity has traditionally been simply considered as a significant risk among non-Hispanic Blacks. However, emerging data seems to suggest that Hispanics, the largest and fastest-growing minority in the USA, might have rates of uncontrolled HTN that significantly exceeds the rates observed for non-Hispanic whites. Unfortunately, paucity of a significant Hispanic representation in major clinical trials has raised significant healthcare concerns regarding our true understanding of the meaning of HTN and associated cardiovascular consequences among this ethnic group. Consequently, there is urgency not only in having a better understanding of HTN among Hispanics, but also to examine the potential factors that may play a role in regulating the expression of HTN and its associated cardiovascular manifestations in this ethnic group.

Chronic Pulmonary Hypertension Causes Significant Interventricular Spatiotemporal Dyssynchrony When Onset of Diastolic Flow Signals Are Assessed by Color M‐Mode

Background: Color M‐mode (CMM) has been useful in characterizing left ventricular (LV) relaxation as well as providing information regarding right ventricular (RV) filling dynamics and pressure gradients. The spatiotemporal resolution of CMM offers a unique opportunity to study the effect of chronic pulmonary hypertension (cPH) on biventricular diastolic function. Methods: Propagation velocities of LV and RV diastolic flows were obtained from 20 individuals with normal pulmonary artery systolic pressures, designated Group I (mean age 50 ± 12 years and 32 ± 6 mmHg) and from 30 patients with cPH, designated Group II (mean age 55 ± 14 years and 81 ± 25 mmHg). Results: Group II patients not only had a significant difference between RV and LV onset of early (13 ± 55 vs. −223 ± 333 msec; P < 0.003) and late (−494 ± 467 vs. −125 ± 258 msec; P < 0.001) diastolic flows; but also had lower propagation velocities of the main RV (40 ± 10 vs. 28 ± 10 cm/sec; P < 0.0001) and LV (52 ± 11 vs. 37 ± 15 cm/sec; P < 0.0003) diastolic flows than Group I individuals. Conclusions: It appears that cPH disrupts not only RV and LV diastolic signal distribution but also their temporal occurrence as well as reducing the propagation velocities of the main diastolic signals in both ventricles. These results seem to imply that cPH causes significant interventricular diastolic dyssynchrony and further studies are now needed to correlate these findings with regard to symptoms and patient clinical outcomes. (Echocardiography 2012;29:653–660)

Effect of cilostazol on platelet reactivity among patients with peripheral artery disease on clopidogrel therapy

Abstract Background: Antiplatelet therapy with clopidogrel is recommended to reduce cardiovascular events in patients with peripheral artery disease (PAD); however, clopidogrel efficacy has not been adequately studied in this patient population. Therefore, we aimed to determine the effects of cilostazol therapy on platelet reactivity among PAD patients on clopidogrel. Methods: We performed a cross-sectional pilot study of 46 Puerto Rican patients diagnosed with PAD. The cohort was divided based on use of clopidogrel and cilostazol (n=24) or clopidogrel alone (n=22). Platelet function was measured ex vivo using the VerifyNow P2Y12 assay. Genomic DNA was extracted from peripheral blood samples using the QIAamp DNA Blood Midi Kit, which was subjected to candidate variant genotyping (CYP2C19, ABCB1, PON1 and P2RY12) using TaqMan quantitative polymerase chain reaction assays. All analyses were performed using SAS version 9.4 (SAS Institute). Results: Among all enrolled patients, 18 (39%) had high on-treatment platelet reactivity (HTPR). The mean platelet reactivity was 207±53 (range, 78–325) with higher P2Y12 reaction units in the non-cilostazol group, 224±45 vs. 191±55 on the cilostazol group (p=0.03). No significant differences were observed in the clinical or genetic variables between the two groups. A multiple regression analysis determined that history of diabetes mellitus (p=0.03), use of cilostazol (p=0.03) and hematocrit (p=0.02) were independent predictors of platelet reactivity. Conclusions: In Puerto Rican PAD patients on clopidogrel therapy, history of diabetes mellitus, use of cilostazol and hematocrit are independent predictors of platelet reactivity. Adjunctive cilostazol therapy may enhance clopidogrel efficacy among PAD patients with HTPR.

Congenital Anastomosis Between Left Anterior Mammary and Pulmonary Vasculatures

Abstract:Several case reports have described the presence of acquired fistula connecting the left internal mammary artery to the pulmonary vasculature; however, occurrence of this type of congenital fistulas is less common. The authors present a case of a congenital left internal mammary artery-pulmonary vasculature fistula that was incidentally found during a coronary angiography in a patient who was being evaluated for coronary artery bypass surgery. The particulars of the case are discussed, and the literature is reviewed.

Massive lipomatous hypertrophy of the right atria.

A case of a 70-year-old female with a history of hypertension, atrial fibrillation, pacer implantation for symptomatic bradycardia, and a prior cerebrovascular accident, and had developed persistent methicillin-sensitive Staphylococcus aureus bacteremia is reported here. As part of her evaluation, a transesophageal echocardiogram was performed, and even though no vegetations were seen on either pacer wires or cardiac valves, a massive homogeneous thickening of the superior portion of the interatrial septum extending to the posterior and roof portions of the right atrial wall as well as to the superior vena cava causing proximal compression of this vessel was noted. Computed tomographic examination of the chest helped to determine that this mass density was not a tumor but in fact intrapericardial fat. Imaging findings and existing literature on this topic are reviewed.

New heart failure reclassification: are we left with more questions than answers?

Cardiovascular diseases continue to be the leading cause of death, accounting for approximately 31% of all deaths worldwide with heart failure (HF) being a growing epidemic since 1997 [1,2]. Current estimates indicate that over 37.7 million people are afflicted with HF worldwide [3,4]. In the US alone, 5.8 million patients carry a diagnosis of HF and 875,000 additional new HF cases are expected each year [5]. The complexity of HF as a chronic long-term condition that continues to deteriorate and is associated with inordinate morbidity and mortality and whose intricate pathophysiology and ever-changing left ventricular (LV) cardiac mechanics are beginning to be comprehended; it has become apparent that the old concept of HF being simply viewed as ‘a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the LV to fill or eject blood’ is no longer applicable [6–8]. The introduction of the HF stage classification was an attempt to better understand the interaction existing between potential risk factors and underlying cardiac structural elements needed for the natural progression of LV dysfunction and symptom development to occur [9]. Not only this stage classification was useful to identify individuals along the natural continuum from those at risk of developing HF to those eventually reaching an advanced HF stage, but also provided physicians with treatment options depending on each individual stage while complementing the already useful New York Heart Association, primarily used to gauge symptom severity and functional limitation [10]. Unfortunately, these steps were not enough as the previously held concept of LV systolic versus diastolic HF continued to be a significant source of controversy and confusion, particularly when both of these mechanical abnormalities could coexist in any given HF patient [11,12]. This debate continued until the American College of Cardiology and the American Heart Association both agreed on making the much easier distinction between preserved (HFpEF) and reduced (HFrEF) not only based on left ventricular ejection fraction (LVEF) but also driven by a wealth of existing data clearly identifying two patient populations with different patient demographics, comorbid clinical profile, response to therapy, and overall prognosis [13]. However, it soon became apparent that a number of patients whose previous LVEF values have ranged >40%, >45%, >50%, and ≥55% did not necessarily fit this new reclassification scheme. Therefore, for the sake of convenience, these patients were further subgrouped. A HFpEF borderline subgroup identified patients with an LVEF between 41% and 49% and whose clinical profile, treatment patterns, and outcomes appeared to be similar to patients with HFpEF, while a HFpEF improved subgroup included patients not only previously diagnosed as HFrEF who now have LVEFs >40% but also are now considered to be clinically distinct from those with persistently preserved or reduced LVEF [13]. Even though this new reclassification is useful as it tries to ease patient identification, it still does not solve the main issue of impact on clinical outcomes, as novel HF therapies have not been up to par with the progression and natural evolution of the disease process and most contemporary HF trials have failed to improve outcomes above standard medical therapy [14,15]. This is certainly relevant among HFpEF as both diagnosis and management of this clinical entity not only has been always clinically challenging, but also therapeutic interventions to reduce symptoms and improve functional capacity as well as other patient-reported outcomes have not shown any significant clinical benefit. An additional burden now being recognized is the overall impact of non-cardiac comorbidities among HF patients. Undoubtedly, as the general population continues to age, survival rates after myocardial infarction leading to LV remodeling continue to increase and a greater proportion of individuals are afflicted with obesity, diabetes, and poorly controlled hypertension and a greater number of HF cases will continue to emerge. This is particularly distressing as approximately 25% of Americans are known to have multiple chronic conditions, an estimate that increases significantly to up 75% in patients with 65 years of age and older [16]. Unfortunately, the clinical impact of chronic comorbid conditions though almost universal among HF patients, it is

Beyond the new blood pressure guidelines: the beat goes on

ABSTRACT The scope of hypertension (HTN) even for those involved in the field is staggering with numbers close to 60 million Americans and more than 1 billion individuals across the globe. It is the most common reason to seek medical attention and according to the World Health Organization, the number one cause of mortality in the world. Yet, we still don’t know what is normal or abnormal. Even though the most recent 2017 Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults has created quite a commotion, new questions could be raised. The purpose of this Editorial not only to fuel more interest on this topic but also to create the notion that HTN needs to be considered a dynamic clinical entity rather than a static blood pressure reading.