Platypnea-Orthodeoxia Syndrome: To Shunt or Not to Shunt, That is the Question.

Platypnea-orthodeoxia syndrome is a rare disease defined by dyspnea and deoxygenation, induced by an upright position, and relieved by recumbency. Causes include shunting through a patent foramen ovale and pulmonary arteriovenous malformations. A 79-year-old woman experienced 2 syncopal episodes at rest and presented at another hospital. In the emergency department, she was hypoxic, needing 6 L/min of oxygen. Her chest radiograph showed nothing unusual. Transthoracic echocardiograms with saline microcavitation evaluation were mildly positive early after agitated-saline administration, suggesting intracardiac shunting. She was then transferred to our center. Right-sided heart catheterization revealed no oximetric evidence of intracardiac shunting while the patient was supine and had a low right atrial pressure. However, her oxygen saturation dropped to 78% when she sat up. Repeat transthoracic echocardiography while sitting revealed a dramatically positive early saline microcavitation-uptake into the left side of the heart. Transesophageal echocardiograms showed a patent foramen ovale, with right-to-left shunting highly dependent upon body position. The patient underwent successful percutaneous patent foramen ovale closure, and her oxygen supplementation was suspended. In patients with unexplained or transient hypoxemia in which a cardiac cause is suspected, it is important to evaluate shunting in both the recumbent and upright positions. In this syndrome, elevated right atrial pressure is not necessary for significant right-to-left shunting. Percutaneous closure, if feasible, is first-line therapy in these patients.

Current and emerging modalities for detection of cardiotoxicity in cardio-oncology.

Advancements in diagnostic tools and curative-intent therapies have improved cancer-specific survival. With prolonged survival, patients are now subject to increased aging and development of cardiovascular risk factors such that further improvements in cancer-specific mortality are at risk of being offset by increased cardiovascular mortality. Moreover, established and novel adjuvant therapies used in cancer treatment are associated with unique and varying degrees of direct as well as indirect myocardial and cardiovascular injury (i.e., cardiotoxicity). Current approaches for evaluating anticancer therapy-induced injury have limitations, particularly lack of sensitivity for early detection of subclinical cardiac and cardiovascular dysfunction. With emerging evidence suggesting early prevention and treatment can mitigate the degree of cardiotoxicity and limit interruption of life-saving cancer therapy, the importance of early detection is increasingly paramount. Newer imaging modalities, functional capacity testing and blood biomarkers have the potential to improve early detection of cardiotoxicity and reduce cardiovascular morbidity and mortality.

Immediate mechanical effects of acute left bundle branch block by speckle tracked strain.

INTRODUCTION: Left bundle branch block (LBBB) is a known complication of transcatheter aortic valve replacement (TAVR) and has been shown to predict worsened outcomes in TAVR patients. A regional longitudinal strain pattern, termed the "classic" pattern of left ventricular (LV) dyssynchrony, which is thought to be due to LBBB, is highly predictive of response to cardiac resynchronization therapy. Whether LBBB causes this "classic" pattern is not known. METHODS: We retrospectively studied patients undergoing TAVR who also underwent pre- and post-TAVR strain analysis to determine if the "classic" pattern arose in those who developed TAVR-induced true LBBB. After removing patients with baseline conduction abnormalities or insufficient studies 9 patients had sufficient data for analysis. Six patients developed LBBB after TAVR and 3 patients did not develop LBBB after TAVR. ECGs were analyzed for the new onset of LBBB after TAVR. Global longitudinal strain (GLS) and regional longitudinal strain patterns were analyzed for changes between pre- and immediately post-TAVR examinations. RESULTS: Patients who did not develop LBBB showed no significant changes in their regional longitudinal strain pattern. Those patients who did develop LBBB showed significant increase in their difference of time-to-onset of contraction between the septal and lateral walls post-TAVR (22 ± 14 ms vs 111 ± 49 ms; p=0.003) and in their difference of time-to-peak contraction between the septal and lateral walls post-TAVR (63 ± 56 ms vs 133 ± 46 ms; p=0.002). Early lateral wall pre-stretch and delayed lateral wall peak contraction emerged in all patients with LBBB but early septal peak contraction meeting the established criteria was present in only one patient. DISCUSSION: The onset of LBBB led to acute, measurable changes in the regional longitudinal strain pattern consisting of early lateral wall pre-stretch and delayed lateral wall peak contraction. These represent 2 of the 3 findings in the "classic" pattern of LV dyssynchrony. Early termination of septal wall contraction meeting established criteria was not routinely found. Time and/or other factors may be required to develop the full "classic" pattern.

Myocardial damage in patients with sarcoidosis and preserved left ventricular systolic function: an observational study.

AIMS: Late gadolinium enhanced cardiovascular magnetic resonance (LGE-CMR) is a valuable test to detect myocardial damage in patients with sarcoidosis; however, the clinical significance of LGE in sarcoidosis patients with preserved left ventricular ejection fraction (LVEF) is not defined. We aim to characterize the prevalence of LGE, its associated cardiac findings, and its clinical implications in sarcoidosis patients with preserved LVEF. METHODS AND RESULTS: One hundred and fifty-two patients with biopsy proven extra-cardiac sarcoidosis, no known cardiac sarcoidosis, and LVEF ≥ 50% referred for LGE-CMR were included in this observational study. The presence of LGE in the left ventricular myocardium was considered diagnostic for cardiac sarcoidosis. The cohort was divided into two groups based on the presence or absence of LGE. Twenty-nine patients (19%) had LGE involving 11 ± 9% of the left ventricle. The modified Japanese Ministry of Health and Welfare (JMHW) criteria for diagnosing cardiac sarcoidosis only had a sensitivity of 52% and specificity of 83% for identifying myocardial LGE in these patients. Compared with those patients without LGE, those with LGE had a higher heart rate (84 ± 19 vs. 76 ± 18 b.p.m., P= 0.002), greater prevalence of an abnormal electrocardiogram (76 vs. 31%, P< 0.001), diastolic dysfunction (67 vs. 33%, P= 0.05), reduced right ventricular ejection fraction (49 ± 8 vs. 55 ± 6%, P= 0.012), and evidence of non-sustained ventricular tachycardia (33 vs. 6%). CONCLUSIONS: In patients with sarcoidosis and preserved systolic function, myocardial damage is commonly present and may increase the risk of ventricular tachy-arrhythmias. The JMHW Criteria were neither sensitive nor specific for predicting the presence of myocardial LGE.