Saad Kubba

Interests

Teaching

Pulmonary Vascular disease,Hemodynamics,Cardiac Imaging,Cardiomyopathy and Heart Failure,Vascular Medicine

Research

Pulmonary Vascular disease,Hemodynamics,Cardiac Imaging,Cardiomyopathy and Heart Failure,Vascular Medicine

Courses

No activities entered.

Scholarly Contributions

Journals/Publications

• Ajmal, M., Javed, B., Kubba, S., Singh, K., Samady, H., Lerman, A., & Corban, M. (2025). Contemporary Review of Myocardial Bridging for Internists. The American journal of medicine, 138(7), 1068-1073.
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  Myocardial bridging is a congenital coronary condition in which an epicardial coronary artery courses within the myocardial muscle instead of running on its surface. Its prevalence varies depending upon the diagnostic modality used for its testing. It is reported to be 40%-80% in autopsy studies, 58% on coronary artery computed tomography, and 0.5%-16% on invasive coronary angiography. Historically, myocardial bridging was considered to be a benign entity. Recent data have shown that this entity not only can cause chronic angina in patients with non-obstructive coronary artery disease but is also associated with an increased risk of major adverse cardiovascular events. Indeed, this condition remains overlooked and not well understood among internal medicine physicians and even among many cardiologists. This review aimed to describe this disease entity and its clinical presentations, understand the anatomic and physiological mechanisms of angina related to this entity, and introduce a comprehensive algorithm for detailed evaluation and phenotype-guided treatment.
• Ajmal, M., Javed, B., Kubba, S., Singh, K., Samady, H., Lerman, A., & Corban, M. (2025). The Reply. American Journal of Medicine, 138(Issue 9). doi:10.1016/j.amjmed.2025.04.016
• Ajmal, M., Javed, B., Kubba, S., Singh, K., Samady, H., Lerman, A., & Corban, M. (2025). The Reply. The American journal of medicine, 138(9), e192-e193.
• Insel, M., El Aini, T., Woodhead, G., Wig, R., Kubba, S., Claessen, G., Howden, E., & Rischard, F. (2025). Post-Pulmonary Embolism Phenotypes Described by Invasive Cardiopulmonary Exercise Testing. Chest, 167(Issue 2). doi:10.1016/j.chest.2024.08.040
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  Background: Post-pulmonary embolism (PE) dyspnea is common. Existing noninvasive studies have demonstrated that post-PE dyspnea is associated with elevations in right ventricular (RV) afterload, dead space ventilation, and deconditioning. We aimed to use invasive cardiopulmonary exercise testing (iCPET) parameters in patients with post-PE dyspnea to identify unique physiologic phenotypes. Research Question: Do distinct post-PE dyspnea physiologic phenotypes exist that are described with iCPET? Study Design and Methods: Patients were enrolled at the time of acute PE and through our pulmonary hypertension (PH) and dyspnea clinic. iCPET was performed if high suspicion existed for PH or if unexplained dyspnea was present. A hierarchical cluster analysis was performed to identify dyspnea phenotypes. iCPET parameters assessing pulmonary hemodynamics, ventilation, and peripheral oxygen use then were compared within and across each cluster and with iCPET control participants against peak oxygen consumed per minute. Results: One hundred seventy-three patients were enrolled. Sixty-seven patients underwent iCPET. All patients showed reductions in peak oxygen consumed per minute and peak cardiac index relative to control participants. Three clusters were identified. Cluster 1 was defined by having elevated RV afterload and impaired ventilatory efficiency. Cluster 2 was defined by elevated RV afterload with reductions in respiratory mechanics. Cluster 3 was defined by mild derangement in RV afterload with mild reductions in peak cardiac output. Interpretation: In this study, iCPET revealed significant heterogeneity in post-PE dyspnea. Three phenotypes were characterized by differences in RV afterload: ventilatory efficiency, respiratory mechanics, and peripheral oxygen use.
• Jothi, S., Insel, M., Claessen, G., Kubba, S., Howden, E. J., Ruiz-Carmona, S., Levine, T., & Rischard, F. P. (2025). Long COVID and chronic fatigue syndrome/myalgic encephalitis share similar pathophysiologic mechanisms of exercise limitation. Physiological Reports, 13(Issue 17). doi:10.14814/phy2.70535
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  Post-acute sequelae of SARS-CoV-2 (PASC or “long COVID”) and chronic fatigue syndrome/myalgic encephalitis (CFS/ME) share symptoms such as exertional dyspnea. We used exercise oxygen pathway analysis, comprising six parameters of oxygen transport and utilization, to identify limiting mechanisms in both conditions. Invasive cardiopulmonary exercise testing was performed on 15 PASC patients, 11 CFS/ME patients, and 11 controls. We evaluated the contributions of alveolar ventilation (V̇a), lung diffusion capacity (DL), cardiac output (Q̇), skeletal muscle diffusion capacity (DM), hemoglobin (Hb), and mitochondrial oxidative phosphorylation (Vmax) to peak oxygen consumption (V̇O2peak). To simulate targeted interventions, each variable was sequentially normalized to assess its impact on V̇O2peak. V̇O2peak was significantly reduced in both PASC and CFS/ME compared to controls. Skeletal muscle O2 diffusion (DM) was the most impaired parameter in both patient groups (p = 0.01). Correcting DM alone improved V̇O2 by 66% in PASC (p = 0.008) and 34.7% in CFS/ME (p = 0.06), suggesting a dominant role for peripheral O2 extraction in exercise limitation. Impaired skeletal muscle oxygen diffusion (DM) is a shared mechanism of exercise intolerance in PASC and CFS/ME and may represent a therapeutic target. However, our findings are limited by small sample size.
• Jothi, S., Insel, M., Claessen, G., Kubba, S., Howden, E. J., Ruiz-Carmona, S., Levine, T., & Rischard, F. P. (2025). Long COVID and chronic fatigue syndrome/myalgic encephalitis share similar pathophysiologic mechanisms of exercise limitation. Physiological reports, 13(17), e70535.
  More info

  Post-acute sequelae of SARS-CoV-2 (PASC or "long COVID") and chronic fatigue syndrome/myalgic encephalitis (CFS/ME) share symptoms such as exertional dyspnea. We used exercise oxygen pathway analysis, comprising six parameters of oxygen transport and utilization, to identify limiting mechanisms in both conditions. Invasive cardiopulmonary exercise testing was performed on 15 PASC patients, 11 CFS/ME patients, and 11 controls. We evaluated the contributions of alveolar ventilation (V̇a), lung diffusion capacity (D ), cardiac output (Q̇), skeletal muscle diffusion capacity (D ), hemoglobin (Hb), and mitochondrial oxidative phosphorylation (V) to peak oxygen consumption (V̇O). To simulate targeted interventions, each variable was sequentially normalized to assess its impact on V̇O. V̇O was significantly reduced in both PASC and CFS/ME compared to controls. Skeletal muscle O diffusion (D ) was the most impaired parameter in both patient groups (p = 0.01). Correcting D alone improved V̇O by 66% in PASC (p = 0.008) and 34.7% in CFS/ME (p = 0.06), suggesting a dominant role for peripheral O extraction in exercise limitation. Impaired skeletal muscle oxygen diffusion (D ) is a shared mechanism of exercise intolerance in PASC and CFS/ME and may represent a therapeutic target. However, our findings are limited by small sample size.
• Uhland, C., Gibbs, A., Insel, M., Kubba, S., & Rischard, F. P. (2025). Treatment Response and Survival in Methamphetamine-Associated Pulmonary Arterial Hypertension. Journal of the American Heart Association, 14(21), e042673.
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  Methamphetamine-associated pulmonary arterial hypertension (Meth-PAH) represents a growing subset of PAH. Relative to idiopathic PAH (iPAH), it is unknown whether patients with Meth-PAH treated with continuous prostacyclin have similar outcomes and treatment response. The aims of this analysis are to evaluate survival, response to therapy, and right ventricle function in similarly treated patients with Meth-PAH and iPAH.
• Uhland, C., Gibbs, A., Insel, M., Kubba, S., & Rischard, F. P. (2025). Treatment Response and Survival in Methamphetamine-Associated Pulmonary Arterial Hypertension. Journal of the American Heart Association, 14(Issue 21). doi:10.1161/jaha.125.042673
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  BACKGROUND: Methamphetamine-associated pulmonary arterial hypertension (Meth-PAH) represents a growing subset of PAH. Relative to idiopathic PAH (iPAH), it is unknown whether patients with Meth-PAH treated with continuous prostacyclin have similar outcomes and treatment response. The aims of this analysis are to evaluate survival, response to therapy, and right ventricle function in similarly treated patients with Meth-PAH and iPAH. METHODS: A prospective protocolized cohort of 138 incident patients (64 Meth-PAH, 74 iPAH) was followed longitudinally, with all patients being treatment-naïve at baseline. Hemodynamic assessments, cardiac imaging, and response to therapy were evaluated. A standardized therapeutic approach involving parenteral subcutaneous treprostinil was applied. Survival was analyzed using Kaplan-Meier and Cox regression. RESULTS: Both groups had similarly advanced PAH at presentation. Improvement in hemodynamics and reduction in European Respiratory Society risk scores were seen over the course of follow-up in both groups. Twenty-nine of 64 (45%) Meth-PAH and 51/74 (69%) of iPAH were initiated on parenteral prostacyclin. During treatment, only 4 patients (2 iPAH and 2 meth-PAH) were taken off treprostinil because of safety concerns. Transplant-free survival was 54/64 (84.4%) for meth-PAH over a mean follow-up time of 46 months and 54/74 (72.9%) for iPAH over a mean follow-up time of 67 months. Additionally, continued methamphetamine use did not adversely affect disease progression or mortality. CONCLUSIONS: Among Meth-PAH patients treated with an aggressive parenteral prostacyclin strategy, there is not a large difference in mortality and treatment response to iPAH. Further research is warranted to explore the long-term effects of methamphetamine use on PAH pathogenesis and outcomes.
• Insel, M., El Aini, T., Woodhead, G., Wig, R., Kubba, S., Claessen, G., Howden, E., & Rischard, F. (2024). Post-Pulmonary Embolism Phenotypes Described by Invasive Cardiopulmonary Exercise Testing. Chest.
  More info

  Post-pulmonary embolism (PE) dyspnea is common. Existing noninvasive studies have demonstrated that post-PE dyspnea is associated with elevations in right ventricular (RV) afterload, dead space ventilation, and deconditioning. We aimed to use invasive cardiopulmonary exercise testing (iCPET) parameters in patients with post-PE dyspnea to identify unique physiologic phenotypes.
• Vanderpool, R. R., Insel, M., Kubba, S., & Rischard, F. P. (2023). The Acute Effects of Prostacyclin on Right Ventricular Contractility and Pulmonary Artery Coupling. American journal of respiratory and critical care medicine.
• Ajmal, M., Kubba, S., Lee, K. S., Lerman, A., & Corban, M. (2022). Abstract 11774: Heart Failure With Preserved Ejection Fraction Secondary to Coronary Endothelial Dysfunction and Microvascular Disease. Circulation, 146(Suppl_1). doi:10.1161/circ.146.suppl_1.11774
• Hershman, M., Singh, A., Kubba, S., Ajmal, M., & Acharya, T. (2021). Statin-Induced Triad of Autoimmune Myocarditis, Myositis, and Transaminitis.. Case reports in cardiology, 2021, 6660362. doi:10.1155/2021/6660362
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  Despite well-established cardiovascular benefits, statins have been associated with myopathic side effects ranging from myalgias to rhabdomyolysis and autoimmune necrotizing myositis. Statins have not been previously shown to cause myocarditis. Our case highlights this rare entity.
• Rischard, F., Vanderpool, R., Kubba, S., Airhart, S., Wickstrom, K., Rosado-Toro, J., & Janardhanan, R. (2018). Abstract 17250: Underestimation of RV Volume by 3D Echocardiography in Patients With Severe PAH. Circulation, 138(Suppl_1). doi:10.1161/circ.138.suppl_1.17250

Proceedings Publications

• Rischard, F., Chatterjee, A., Insel, M., Kubba, S., Habib, N., Sher, N., Tandon, A., & Seckeler, M. (2022). To Drain or Not to Drain: Hemodynamic Characterization of Tamponade in PAH. In ATS.
• Rischard, F., Kubba, S., Uhland, C., Insel, M., & Stroud, S. (2022). Oxygen Utilization as a Primary Mediator of Age-Related Functional Decline in Pulmonary Arterial Hypertension. In ATS.
• Janardhanan, R., Desai, A., Kubba, S., Airhart, S., Wickstrom, K., Rosado-Toro, J., Vanderpool, R., & Rischard, F. (2019). The Inaccuracy of Right Ventricular 3d Echocardiography Is Accentuated by Disease Severity in Pulmonary Arterial Hypertension. In ATS.
• Yuan, J., Janardhanan, R., Kubba, S., Erickson, H., Vanderpool, R., Holmathchi, J., Puri, R., Airhart, S., Lizarraga, A., Hansen, L., Naeije, R., Garcia, J., & Rischard, F. (2019). Ratio of Stroke Volume to End-Systolic Volume Predicts Change in Right Ventricular Ejection Fraction in Patients with Pulmonary Arterial Hypertension. In ATS.

Presentations

• Kubba, S. (2024, June). Combined Echocardiography - CPET. AZ Echo Meeting. Tucson Medical Center Marshall Conference Room: The Arizona Society of Echocardiography.
• Kubba, S. (2023, October). Pulmonary Hypertension. Sarver Heart Failure Symposium 2023. Health Sciences Innovation Building, Univeristy of Arizona, Tucson, AZ: Sarver Heart Center.
• Kubba, S. (2023, October). Timely Referral. Sarver Heart Center Symposium 2023. Health Sciences Innovation Building, Univeristy of Arizona, Tucson, AZ: Sarver Heart Center.
• Habib, N., Sher, A., Tandon, S., Kubba, S., Insel, M., Chatterjee, A., Seckeler, M., & Rischard, F. (2022, May). To Drain or Not to Drain: Hemodynamic Charcterization of Tamponade in Pulmonary Arterial Hypertension. American Thoracic Society 2022. San Francisco, CA.
• Kubba, S. (2022). Debate Presentation, Sodium Restriction in Heart Failure. American College of Cardiology - Arizona.
• Uhland, C., Insel, M., Stroud, S. C., Kubba, S., & Rischard, F. (2022, May). Oxygen Utilization as a Primary Mediator of Age-Related Functional Decline in Pulmonary Arterial Hypertension. American Thoracic Society 2022. San Francisco, CA.

Poster Presentations

• Ajmal, M., Kubba, S., Lee, K. S., Lerman, A., & Corban, M. (2022, November). Abstract 11774: Heart Failure with Preserved Ejection Fraction Secondary to Coronary Endothelial Dysfunction and Microvascular Disease. American Heart Association Scientific Sessions 2022. Chicago, IL.
• Badagliacca, R., Rischard, F., Papa, S., Kubba, S., Vanderpool, R., Yuan, J., Garcia, J., Airhart, S., Poscia, R., Pezzuto, B., Manzi, G., Sciomer, S., Torre, R., Fedele, F., & Vizza, C. (2019, April). Clinical Implications of Idiopathic Pulmonary Arterial Hypertension Phenotypes Defined by Cluster Analysis. International Society for Heart and Lung Transplantation 2019. Orlando, FL.
• Keeley Ravellette, K., Kubba, S., Airhart, S., Yuan, J., Rischard, F., & Vanderpool, R. (2019, April). Increased Pulmonary Vascular Impedance in Patients with Severe Pulmonary Arterial Hypertension. Experimental Biology 2019. Orlando, FL.
• Kubba, S., Airhart, S., Wickstrom, K., Rosado-Toro, J., Desai, A., Janardhanan, R., Vanderpool, R., & Rischard, F. (2019, May). The Inaccuracy of Right Ventricular 3d Echocardiography Is Accentuated by Disease Severity in Pulmonary Arterial Hypertension. American Thoracic Society 2019. Dallas, TX.
• Vanderpool, R., Holmathchi, J., Puri, R., Airhart, S., Erickson, H., Lizarraga, A., Hansen, L., Kubba, S., Janardhanan, R., Naeije, R., Garcia, J., Yuan, J., & Rischard, F. (2019, May). Ratio of Stroke Volume to End-Systolic Volume Predicts Change in Right Ventricular Ejection Fraction in Patients with Pulmonary Arterial Hypertension. American Thoracic Society 2019. Dallas, TX.
• Kubba, S., Airhart, S., Wickstrom, K., Rosado-Toro, J., Janardhanan, R., Vanderpool, R., & Rischard, F. (2018, spring). Underestimation of RV Volume by 3D Echocardiography in Patients With Severe PAH. American Heart Association Annual Scientific Session 2018. Chicago, IL.

Other Teaching Materials

• Kubba, S. (2024. 2024 CCU Handbook for Internal Medicine Residents, Supervisor. University of Arizona.